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[PMID]:29277915
[Au] Autor:Zhang X; Ping HY; Li JH; Duan SX; Jiang XW
[Ad] Endereço:Department of Pediatric Surgery, The Affiliated Maternal and Child Health Hospital of Shenzhen University Medical College, Shenzhen, China.
[Ti] Título:Diethylstilbestrol regulates mouse gubernaculum testis cell proliferation via PLC-Ca -CREB pathway.
[So] Source:Cell Biochem Funct;36(1):13-17, 2018 Jan.
[Is] ISSN:1099-0844
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Recent evidence suggested a positive correlation between environmental estrogens (EEs) and high incidence of abnormalities in male urogenital system, but the mechanism remains unclear. Diethylstilbestrol (DES) is a nonsteroidal synthetic estrogen that disrupts the morphology and proliferation of gubernaculum testis cells, but the underlying mechanism is unclear. In this study, mouse gubernaculum testis cells were pretreated with phospholipase C (PLC) inhibitor U-73122 and then treated with DES. The results demonstrated that U-73122 impaired DES-evoked intracellular Ca2+ mobilization in gubernaculum testis cells and inhibited DES-induced proliferation of gubernaculum testis cells. Mechanistically, we found that U-73122 inhibited DES-induced activation of cAMP-response element binding protein (CREB) in gubernaculum testis cells. In conclusion, these data suggest that the effects of DES on mouse gubernaculum testis cells are mediated by PLC-Ca -CREB pathway. SIGNIFICANCE OF THE STUDY: Environmental estrogens remain a serious threat to male reproductive health, and it is important to understand the mechanism by which EEs affect the male productive system. Here we explore potential mechanisms how the proliferation and contractility of gubernaculum testis cells are regulated by diethylstilbestrol. Our findings provide the first evidence that PLC-Ca -CREB signalling pathway mediates the nongenomic effects of diethylstilbestrol on gubernaculum testis cells. These findings provide new insight into the role of diethylstilbestrol in the aetiology of male reproductive dysfunction and will help develop better approaches for the prevention and therapy of male reproductive malformation.
[Mh] Termos MeSH primário: Cálcio/metabolismo
Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo
Dietilestilbestrol/farmacologia
Gubernáculo/efeitos dos fármacos
Testículo/efeitos dos fármacos
Fosfolipases Tipo C/metabolismo
[Mh] Termos MeSH secundário: Animais
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Estrenos/farmacologia
Gubernáculo/citologia
Gubernáculo/metabolismo
Masculino
Camundongos
Pirrolidinonas/farmacologia
Testículo/citologia
Testículo/metabolismo
Fosfolipases Tipo C/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclic AMP Response Element-Binding Protein); 0 (Estrenes); 0 (Pyrrolidinones); 112648-68-7 (1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione); 731DCA35BT (Diethylstilbestrol); EC 3.1.4.- (Type C Phospholipases); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE
[do] DOI:10.1002/cbf.3312


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[PMID]:29364921
[Au] Autor:Nowak M; Boos A; Kowalewski MP
[Ad] Endereço:Institute of Veterinary Anatomy, Vetsuisse Faculty, University of Zurich, Zurich, Switzerland.
[Ti] Título:Luteal and hypophyseal expression of the canine relaxin (RLN) system during pregnancy: Implications for luteotropic function.
[So] Source:PLoS One;13(1):e0191374, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:By acting through its receptors (RXFP1, RXFP2), relaxin (RLN) exerts species-specific effects during pregnancy; possible luteotropic effects through stimulation of prolactin (PRL) release have been suggested. In the domestic dog (Canis lupus familiaris) serum PRL increases in pregnant bitches shortly after RLN appears in the circulation, and a possible functional relationship between the RLN and the PRL systems in regulating progesterone secretion has been implied. Therefore, here (Study 1) the luteal expression and localization of the RLN system was investigated by immunohistochemistry using custom-made antibodies and semi-quantitative PCR, at selected time points during gestation: pre-implantation (d. 8-12), post-implantation (d. 18-25), mid-gestation (d. 35-40) and at normal and antigestagen-induced luteolysis. Further, (Study 2) hypophyseal expression of the RLN system and its spatial association with PRL was assessed. Luteal expression of RLN, but not of its receptors, was time-dependent: it increased significantly following implantation towards mid-gestation and decreased at prepartum. Antigestagen treatment resulted in downregulation of RLN and RXFP2. Whereas RLN was localized in steroidogenic cells, RXFP1 and RXFP2 also stained strongly in macrophages and vascular endothelial cells. The RLN system was detected in the canine adenohypophysis and was co-localized with PRL in hypophyseal lactotrophs. The intraluteal RLN seems to be involved in regulating the canine corpus luteum (CL) in a time-dependent manner. The presence of RLN family members in the adenohypophysis implies their possible involvement in regulating the availability of PRL and other pituitary hormones.
[Mh] Termos MeSH primário: Corpo Lúteo/fisiologia
Hipófise/fisiologia
Relaxina/fisiologia
[Mh] Termos MeSH secundário: Animais
Manutenção do Corpo Lúteo/genética
Manutenção do Corpo Lúteo/fisiologia
Cães
Estrenos/farmacologia
Feminino
Expressão Gênica/efeitos dos fármacos
Imuno-Histoquímica
Modelos Biológicos
Gravidez
Prolactina/sangue
Prolactina/fisiologia
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Receptores Acoplados a Proteínas-G/genética
Receptores Acoplados a Proteínas-G/fisiologia
Receptores de Peptídeos/genética
Receptores de Peptídeos/fisiologia
Relaxina/sangue
Relaxina/genética
Especificidade da Espécie
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Estrenes); 0 (RNA, Messenger); 0 (Receptors, G-Protein-Coupled); 0 (Receptors, Peptide); 0 (relaxin receptors); 0UT4JLE1CM (aglepristone); 9002-62-4 (Prolactin); 9002-69-1 (Relaxin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180125
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191374


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[PMID]:28445587
[Au] Autor:Alonso B; Bartolomé-Martín D; Ferrero JJ; Ramírez-Franco J; Torres M; Sánchez-Prieto J
[Ad] Endereço:Departamento de Bioquímica, Facultad de Veterinaria, Universidad Complutense, Madrid, Spain.
[Ti] Título:CB1 receptors down-regulate a cAMP/Epac2/PLC pathway to silence the nerve terminals of cerebellar granule cells.
[So] Source:J Neurochem;142(3):350-364, 2017 Aug.
[Is] ISSN:1471-4159
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cannabinoid receptors mediate short-term retrograde inhibition of neurotransmitter release, as well as long-term depression of synaptic transmission at excitatory synapses. The responses of individual nerve terminals in VGLUT1-pHluorin transfected cerebellar granule cells to cannabinoids have shown that prolonged activation of cannabinoid type 1 receptors (CB1Rs) silences a subpopulation of previously active synaptic boutons. Adopting a combined pharmacological and genetic approach to study the molecular mechanisms of CB1R-induced silencing, we found that adenylyl cyclase inhibition decreases cAMP levels while it increases the number of silent synaptic boutons and occludes the induction of further silencing by the cannabinoid agonist HU-210. Guanine nucleotide exchange proteins directly activated by cAMP (Epac proteins) mediate some of the presynaptic effects of cAMP in the potentiation of synaptic transmission. ESI05, a selective Epac2 inhibitor, and U-73122, the specific inhibitor of phospholipase C (PLC), both augment the number of silent synaptic boutons. Moreover, they abolish the capacity of the Epac activator, 8-(4-chlorophenylthio)-2'-O-methyladenosine 3',5'-cyclic monophosphate monosodium hydrate, to prevent HU-210-induced silencing consistent with PLC signaling lying downstream of Epac2 proteins. Furthermore, Rab3-interacting molecule (RIM)1α KO cells have many more basally silent synaptic boutons (12.9 ± 3.5%) than wild-type cells (1.1 ± 0.5%). HU-210 induced further silencing in these mutant cells, although 8-(4-chlorophenylthio)-2'-O-methyladenosine 3',5'-cyclic monophosphate monosodium hydrate only awoke the HU-210-induced silence and not the basally silent synaptic boutons. This behavior can be rescued by expressing RIM1α in RIM1α KO cells, these cells behaving very much like wild-type cells. These findings support the hypothesis that a cAMP/Epac/PLC signaling pathway targeting the release machinery appears to mediate cannabinoid-induced presynaptic silencing.
[Mh] Termos MeSH primário: Cerebelo/citologia
Neurônios/metabolismo
Receptor CB1 de Canabinoide/metabolismo
Transmissão Sináptica/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Cerebelo/efeitos dos fármacos
AMP Cíclico/metabolismo
Regulação para Baixo/efeitos dos fármacos
Estrenos/farmacologia
Feminino
Fatores de Troca do Nucleotídeo Guanina/metabolismo
Masculino
Neurônios/efeitos dos fármacos
Pirrolidinonas/farmacologia
Ratos Wistar
Receptor CB1 de Canabinoide/efeitos dos fármacos
Sinapses/efeitos dos fármacos
Sinapses/metabolismo
Transmissão Sináptica/fisiologia
Fosfolipases Tipo C/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (EPAC protein, rat); 0 (Estrenes); 0 (Guanine Nucleotide Exchange Factors); 0 (Pyrrolidinones); 0 (Receptor, Cannabinoid, CB1); 112648-68-7 (1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione); E0399OZS9N (Cyclic AMP); EC 3.1.4.- (Type C Phospholipases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170921
[Lr] Data última revisão:
170921
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170427
[St] Status:MEDLINE
[do] DOI:10.1111/jnc.14059


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[PMID]:28444736
[Au] Autor:Murji A; Whitaker L; Chow TL; Sobel ML
[Ad] Endereço:Department of Obstetrics and Gynecology, Mount Sinai Hospital, University of Toronto, 700 University Ave - 3rd Floor, Toronto, ON, Canada, M5G 1Z5.
[Ti] Título:Selective progesterone receptor modulators (SPRMs) for uterine fibroids.
[So] Source:Cochrane Database Syst Rev;4:CD010770, 2017 Apr 26.
[Is] ISSN:1469-493X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Uterine fibroids are smooth muscle tumours arising from the uterus. These tumours, although benign, are commonly associated with abnormal uterine bleeding, bulk symptoms and reproductive dysfunction. The importance of progesterone in fibroid pathogenesis supports selective progesterone receptor modulators (SPRMs) as effective treatment. Both biochemical and clinical evidence suggests that SPRMs may reduce fibroid growth and ameliorate symptoms. SPRMs can cause unique histological changes to the endometrium that are not related to cancer, are not precancerous and have been found to be benign and reversible. This review summarises randomised trials conducted to evaluate the effectiveness of SPRMs as a class of medication for treatment of individuals with fibroids. OBJECTIVES: To evaluate the effectiveness and safety of SPRMs for treatment of premenopausal women with uterine fibroids. SEARCH METHODS: We searched the Specialised Register of the Cochrane Gynaecology and Fertility Group, the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, Embase, PsycINFO, the Cumulative Index to Nursing and Allied Health Literature (CINAHL) and clinical trials registries from database inception to May 2016. We handsearched the reference lists of relevant articles and contacted experts in the field to request additional data. SELECTION CRITERIA: Included studies were randomised controlled trials (RCTs) of premenopausal women with fibroids who were treated for at least three months with a SPRM. DATA COLLECTION AND ANALYSIS: Two review authors independently reviewed all eligible studies identified by the search. We extracted data and assessed risk of bias independently using standard forms. We analysed data using mean differences (MDs) or standardised mean differences (SMDs) for continuous data and odds ratios (ORs) for dichotomous data. We performed meta-analyses using the random-effects model. Our primary outcome was change in fibroid-related symptoms. MAIN RESULTS: We included in the review 14 RCTs with a total of 1215 study participants. We could not extract complete data from three studies. We included in the meta-analysis 11 studies involving 1021 study participants: 685 received SPRMs and 336 were given a control intervention (placebo or leuprolide). Investigators evaluated three SPRMs: mifepristone (five studies), ulipristal acetate (four studies) and asoprisnil (two studies). The primary outcome was change in fibroid-related symptoms (symptom severity, health-related quality of life, abnormal uterine bleeding, pelvic pain). Adverse event reporting in the included studies was limited to SPRM-associated endometrial changes. More than half (8/14) of these studies were at low risk of bias in all domains. The most common limitation of the other studies was poor reporting of methods. The main limitation for the overall quality of evidence was potential publication bias. SPRM versus placebo SPRM treatment resulted in improvements in fibroid symptom severity (MD -20.04 points, 95% confidence interval (CI) -26.63 to -13.46; four RCTs, 171 women, I = 0%; moderate-quality evidence) and health-related quality of life (MD 22.52 points, 95% CI 12.87 to 32.17; four RCTs, 200 women, I = 63%; moderate-quality evidence) on the Uterine Fibroid Symptom Quality of Life Scale (UFS-QoL, scale 0 to 100). Women treated with an SPRM showed reduced menstrual blood loss on patient-reported bleeding scales, although this effect was small (SMD -1.11, 95% CI -1.38 to -0.83; three RCTs, 310 women, I = 0%; moderate-quality evidence), along with higher rates of amenorrhoea (29 per 1000 in the placebo group vs 237 to 961 per 1000 in the SPRM group; OR 82.50, 95% CI 37.01 to 183.90; seven RCTs, 590 women, I = 0%; moderate-quality evidence), compared with those given placebo. We could draw no conclusions regarding changes in pelvic pain owing to variability in the estimates. With respect to adverse effects, SPRM-associated endometrial changes were more common after SPRM therapy than after placebo (OR 15.12, 95% CI 6.45 to 35.47; five RCTs, 405 women, I = 0%; low-quality evidence). SPRM versus leuprolide acetate In comparing SPRM versus other treatments, two RCTs evaluated SPRM versus leuprolide acetate. One RCT reported primary outcomes. No evidence suggested a difference between SPRM and leuprolide groups for improvement in quality of life, as measured by UFS-QoL fibroid symptom severity scores (MD -3.70 points, 95% CI -9.85 to 2.45; one RCT, 281 women; moderate-quality evidence) and health-related quality of life scores (MD 1.06 points, 95% CI -5.73 to 7.85; one RCT, 281 women; moderate-quality evidence). It was unclear whether results showed a difference between SPRM and leuprolide groups for reduction in menstrual blood loss based on the pictorial blood loss assessment chart (PBAC), as confidence intervals were wide (MD 6 points, 95% CI -40.95 to 50.95; one RCT, 281 women; low-quality evidence), or for rates of amenorrhoea (804 per 1000 in the placebo group vs 732 to 933 per 1000 in the SPRM group; OR 1.14, 95% CI 0.60 to 2.16; one RCT, 280 women; moderate-quality evidence). No evidence revealed differences between groups in pelvic pain scores based on the McGill Pain Questionnaire (scale 0 to 45) (MD -0.01 points, 95% CI -2.14 to 2.12; 281 women; moderate-quality evidence). With respect to adverse effects, SPRM-associated endometrial changes were more common after SPRM therapy than after leuprolide treatment (OR 10.45, 95% CI 5.38 to 20.33; 301 women; moderate-quality evidence). AUTHORS' CONCLUSIONS: Short-term use of SPRMs resulted in improved quality of life, reduced menstrual bleeding and higher rates of amenorrhoea than were seen with placebo. Thus, SPRMs may provide effective treatment for women with symptomatic fibroids. Evidence derived from one RCT showed no difference between leuprolide acetate and SPRM with respect to improved quality of life and bleeding symptoms. Evidence was insufficient to show whether effectiveness was different between SPRMs and leuprolide. Investigators more frequently observed SPRM-associated endometrial changes in women treated with SPRMs than in those treated with placebo or leuprolide acetate. As noted above, SPRM-associated endometrial changes are benign, are not related to cancer and are not precancerous. Reporting bias may impact the conclusion of this meta-analysis. Well-designed RCTs comparing SPRMs versus other treatments are needed.
[Mh] Termos MeSH primário: Antineoplásicos Hormonais/uso terapêutico
Estrenos/uso terapêutico
Leiomioma/tratamento farmacológico
Mifepristona/uso terapêutico
Norpregnadienos/uso terapêutico
Oximas/uso terapêutico
Receptores de Progesterona/antagonistas & inibidores
Neoplasias Uterinas/tratamento farmacológico
[Mh] Termos MeSH secundário: Amenorreia/tratamento farmacológico
Feminino
Seres Humanos
Leuprolida/uso terapêutico
Menstruação/efeitos dos fármacos
Dor Pélvica/tratamento farmacológico
Qualidade de Vida
Ensaios Clínicos Controlados Aleatórios como Assunto
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents, Hormonal); 0 (Estrenes); 0 (Norpregnadienes); 0 (Oximes); 0 (Receptors, Progesterone); 320T6RNW1F (Mifepristone); 72W09924WP (asoprisnil); EFY6W0M8TG (Leuprolide); YF7V70N02B (ulipristal acetate)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170427
[St] Status:MEDLINE
[do] DOI:10.1002/14651858.CD010770.pub2


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[PMID]:28442571
[Au] Autor:Galaz-Montoya M; Wright SJ; Rodriguez GJ; Lichtarge O; Wensel TG
[Ad] Endereço:From the Verna and Marrs McLean Department of Biochemistry and Molecular Biology and.
[Ti] Título:ß -Adrenergic receptor activation mobilizes intracellular calcium via a non-canonical cAMP-independent signaling pathway.
[So] Source:J Biol Chem;292(24):9967-9974, 2017 Jun 16.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Beta adrenergic receptors (ßARs) are G-protein-coupled receptors essential for physiological responses to the hormones/neurotransmitters epinephrine and norepinephrine which are found in the nervous system and throughout the body. They are the targets of numerous widely used drugs, especially in the case of the most extensively studied ßAR, ß AR, whose ligands are used for asthma and cardiovascular disease. ßARs signal through Gα G-proteins and via activation of adenylyl cyclase and cAMP-dependent protein kinase, but some alternative downstream pathways have also been proposed that could be important for understanding normal physiological functioning of ßAR signaling and its disruption in disease. Using fluorescence-based Ca flux assays combined with pharmacology and gene knock-out methods, we discovered a previously unrecognized endogenous pathway in HEK-293 cells whereby ß AR activation leads to robust Ca mobilization from intracellular stores via activation of phospholipase C and opening of inositol trisphosphate (InsP ) receptors. This pathway did not involve cAMP, Gα , or Gα or the participation of the other members of the canonical ß AR signaling cascade and, therefore, constitutes a novel signaling mechanism for this receptor. This newly uncovered mechanism for Ca mobilization by ß AR has broad implications for adrenergic signaling, cross-talk with other signaling pathways, and the effects of ßAR-directed drugs.
[Mh] Termos MeSH primário: Sinalização do Cálcio
Retículo Endoplasmático/metabolismo
Epinefrina/metabolismo
Receptores de Inositol 1,4,5-Trifosfato/agonistas
Norepinefrina/metabolismo
Fosfoinositídeo Fosfolipase C/metabolismo
Receptores Adrenérgicos beta 2/metabolismo
[Mh] Termos MeSH secundário: Agonistas Adrenérgicos beta/farmacologia
Compostos de Boro/farmacologia
Sistemas CRISPR-Cas
Bloqueadores dos Canais de Cálcio/farmacologia
Sinalização do Cálcio/efeitos dos fármacos
Retículo Endoplasmático/efeitos dos fármacos
Retículo Endoplasmático/enzimologia
Ativação Enzimática/efeitos dos fármacos
Inibidores Enzimáticos/farmacologia
Estrenos/farmacologia
Células HEK293
Seres Humanos
Receptores de Inositol 1,4,5-Trifosfato/antagonistas & inibidores
Receptores de Inositol 1,4,5-Trifosfato/metabolismo
Isoproterenol/farmacologia
Cinética
Fosfoinositídeo Fosfolipase C/antagonistas & inibidores
Fosfoinositídeo Fosfolipase C/química
Pirrolidinonas/farmacologia
Receptores Adrenérgicos beta 2/química
Receptores Adrenérgicos beta 2/genética
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/metabolismo
ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/antagonistas & inibidores
ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/química
ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/metabolismo
Tapsigargina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-aminoethyl diphenylborinate); 0 (ADRB2 protein, human); 0 (Adrenergic beta-Agonists); 0 (Boron Compounds); 0 (Calcium Channel Blockers); 0 (Enzyme Inhibitors); 0 (Estrenes); 0 (ITPR1 protein, human); 0 (Inositol 1,4,5-Trisphosphate Receptors); 0 (Pyrrolidinones); 0 (Receptors, Adrenergic, beta-2); 0 (Recombinant Fusion Proteins); 112648-68-7 (1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione); 67526-95-8 (Thapsigargin); EC 3.1.4.11 (Phosphoinositide Phospholipase C); EC 3.6.3.8 (Sarcoplasmic Reticulum Calcium-Transporting ATPases); L628TT009W (Isoproterenol); X4W3ENH1CV (Norepinephrine); YKH834O4BH (Epinephrine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170924
[Lr] Data última revisão:
170924
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170427
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.787119


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[PMID]:28223151
[Au] Autor:Ruamyod K; Watanapa WB; Shayakul C
[Ad] Endereço:Department of Physiology Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, 10700, Thailand. Electronic address: katesirin.ruy@mahidol.ac.th.
[Ti] Título:Testosterone rapidly increases Ca -activated K currents causing hyperpolarization in human coronary artery endothelial cells.
[So] Source:J Steroid Biochem Mol Biol;168:118-126, 2017 Apr.
[Is] ISSN:1879-1220
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Testosterone has endothelium-dependent vasodilatory effects on the coronary artery, with some reports suggesting endothelial ion channel involvement. This study employed the whole-cell patch clamp technique to investigate the effect of testosterone on ion channels in human coronary artery endothelial cells (HCAECs) and the mechanisms involved. We found that 0.03-3µM testosterone significantly induced a rapid, concentration-dependent increase in total HCAEC current (EC , 71.96±1.66nM; maximum increase, 59.13±8.37%; mean±SEM). The testosterone-enhanced currents consisted of small- and large-conductance Ca -activated K currents (SK and BK currents), but not Cl and nonselective cation currents. Either a non-permeant testosterone conjugate or the non-aromatizable androgen dihydrotestosterone (DHT) could increase HCAEC currents as well. The androgen receptor antagonist flutamide prevented this testosterone, testosterone conjugate, and DHT effect, while the estrogen receptor antagonist fulvestrant did not. Incubating HCAECs with pertussis toxin or protein kinase A inhibitor H-89 largely inhibited the testosterone effect, while pre-incubation with phospholipase C inhibitor U-73122, prostacyclin inhibitor indomethacin, nitric oxide synthase inhibitor L-NAME or cytochrome P450 inhibitor MS-PPOH, did not. Finally, testosterone application induced HCAEC hyperpolarization within minutes; this effect was prevented by SK and BK current inhibitors apamin and iberiotoxin. This is the first electrophysiological demonstration of androgen-induced K current increase, leading to hyperpolarization, in any endothelial cell, and the first report of SK as a testosterone target. Our data show that testosterone rapidly increased whole-cell HCAEC SK and BK currents via a surface androgen receptor, G protein, and protein kinase A. This mechanism may explain rapid testosterone-induced coronary vasodilation seen in vivo.
[Mh] Termos MeSH primário: Vasos Coronários/citologia
Células Endoteliais/metabolismo
Subunidades alfa Gi-Go de Proteínas de Ligação ao GTP/metabolismo
Canais de Potássio Cálcio-Ativados/metabolismo
Testosterona/sangue
[Mh] Termos MeSH secundário: Androgênios/química
Apamina/química
Linhagem Celular
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
Células Endoteliais/efeitos dos fármacos
Epoprostenol/antagonistas & inibidores
Estrenos/química
Seres Humanos
Indometacina/química
NG-Nitroarginina Metil Éster/química
Óxido Nítrico Sintase/química
Pirrolidinonas/química
Receptores Androgênicos/metabolismo
Transdução de Sinais
Testosterona/química
Vasodilatação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Androgens); 0 (Estrenes); 0 (Potassium Channels, Calcium-Activated); 0 (Pyrrolidinones); 0 (Receptors, Androgen); 112648-68-7 (1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione); 24345-16-2 (Apamin); 3XMK78S47O (Testosterone); DCR9Z582X0 (Epoprostenol); EC 1.14.13.39 (Nitric Oxide Synthase); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); EC 3.6.5.1 (GTP-Binding Protein alpha Subunits, Gi-Go); V55S2QJN2X (NG-Nitroarginine Methyl Ester); XXE1CET956 (Indomethacin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170704
[Lr] Data última revisão:
170704
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170223
[St] Status:MEDLINE


  7 / 2830 MEDLINE  
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[PMID]:28125813
[Au] Autor:Khin PP; Zaw TS; Sohn UD
[Ad] Endereço:Department of Pharmacology, College of Pharmacy, Chung-Ang University, Seoul, Republic of Korea.
[Ti] Título:Signal Transduction Underlying the Inhibitory Mechanism of Fluoxetine on Electrical Field Stimulation Response in Rat Ileal Smooth Muscle.
[So] Source:Pharmacology;99(5-6):216-225, 2017.
[Is] ISSN:1423-0313
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Fluoxetine (FLX), a well-known antidepressant drug under the class of selective serotonin reuptake inhibitor, exerts its action by inhibiting the reuptake of serotonin selectively. In some studies, it has been demonstrated that FLX relaxes the intestinal smooth muscle. In this study, we aimed at studying the signal transduction pathway underlying the muscle relaxation effect of FLX on electrically stimulated rat ileal muscle contraction. To investigate the possible mechanism involved, various antagonists were used. It was found that inhibition with L-NG-nitroarginine methyl ester, ondansetron, GR113808 and bicuculline enhanced the relaxation effect of FLX. However, the effect of FLX was nullified under the presence of atropine, calcium channel modulator (calcium ionophore A23187), and potassium channel blockers (tetraethylammonium chloride, 4-aminopyridine and glybenclamide). Specific pathway-inhibiting antagonists, Y27632 (Rho-kinase inhibitor) and U73122 (phospholipase-C inhibitor) reversed the antagonistic effect of FLX, while ML-9 (myosin light chain kinase inhibitor) and chelerythrine (protein kinase C inhibitor) augmented the FLX-induced inhibition effect. Taken together, we concluded that FLX exerts the inhibitory effect on electric field stimulation response in rat ileal smooth muscle by the inhibition of muscarinic receptors, decrease of intracellular calcium level by inhibiting phospholipase C and opens the potassium channels.
[Mh] Termos MeSH primário: Fluoxetina/farmacologia
Íleo/efeitos dos fármacos
Contração Muscular/efeitos dos fármacos
Músculo Liso/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: 4-Aminopiridina/farmacologia
Amidas/farmacologia
Animais
Atropina/farmacologia
Azepinas/farmacologia
Benzofenantridinas/farmacologia
Bicuculina/farmacologia
Calcimicina/farmacologia
Interações Medicamentosas
Estimulação Elétrica
Estrenos/farmacologia
Fluoxetina/antagonistas & inibidores
Glibureto/farmacologia
Íleo/fisiologia
Técnicas In Vitro
Indóis/farmacologia
Masculino
Contração Muscular/fisiologia
Músculo Liso/fisiologia
NG-Nitroarginina Metil Éster/farmacologia
Ondansetron/farmacologia
Piridinas/farmacologia
Pirrolidinonas/farmacologia
Ratos
Sulfonamidas/farmacologia
Tetraetilamônio/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amides); 0 (Azepines); 0 (Benzophenanthridines); 0 (Estrenes); 0 (Indoles); 0 (Pyridines); 0 (Pyrrolidinones); 0 (Sulfonamides); 01K63SUP8D (Fluoxetine); 105637-50-1 (ML 9); 112648-68-7 (1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione); 138381-45-0 (Y 27632); 37H9VM9WZL (Calcimycin); 4AF302ESOS (Ondansetron); 66-40-0 (Tetraethylammonium); 7C0697DR9I (Atropine); BH3B64OKL9 (4-Aminopyridine); E3B045W6X0 (chelerythrine); SX6K58TVWC (Glyburide); V55S2QJN2X (NG-Nitroarginine Methyl Ester); Y37615DVKC (Bicuculline); ZT350OYT3I (GR 113808)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170127
[St] Status:MEDLINE
[do] DOI:10.1159/000449528


  8 / 2830 MEDLINE  
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[PMID]:28062485
[Au] Autor:Gu QD; Joe DS; Gilbert CA
[Ad] Endereço:Division of Basic Medical Sciences, Mercer University School of Medicine, Macon, Georgia gu_q@mercer.edu.
[Ti] Título:Activation of bitter taste receptors in pulmonary nociceptors sensitizes TRPV1 channels through the PLC and PKC signaling pathway.
[So] Source:Am J Physiol Lung Cell Mol Physiol;312(3):L326-L333, 2017 Mar 01.
[Is] ISSN:1522-1504
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bitter taste receptors (T2Rs), a G protein-coupled receptor family capable of detecting numerous bitter-tasting compounds, have recently been shown to be expressed and play diverse roles in many extraoral tissues. Here we report the functional expression of T2Rs in rat pulmonary sensory neurons. In anesthetized spontaneously breathing rats, intratracheal instillation of T2R agonist chloroquine (10 mM, 0.1 ml) significantly augmented chemoreflexes evoked by right-atrial injection of capsaicin, a specific activator for transient receptor potential vanilloid receptor 1 (TRPV1), whereas intravenous infusion of chloroquine failed to significantly affect capsaicin-evoked reflexes. In patch-clamp recordings with isolated rat vagal pulmonary sensory neurons, pretreatment with chloroquine (1-1,000 µM, 90 s) concentration dependently potentiated capsaicin-induced TRPV1-mediated inward currents. Preincubating with diphenitol and denatonium (1 mM, 90 s), two other T2R activators, also enhanced capsaicin currents in these neurons but to a lesser extent. The sensitizing effect of chloroquine was effectively prevented by the phospholipase C inhibitor U73122 (1 µM) or by the protein kinase C inhibitor chelerythrine (10 µM). In summary, our study showed that activation of T2Rs augments capsaicin-evoked TRPV1 responses in rat pulmonary nociceptors through the phospholipase C and protein kinase C signaling pathway.
[Mh] Termos MeSH primário: Pulmão/metabolismo
Nociceptores/metabolismo
Proteína Quinase C/metabolismo
Receptores Acoplados a Proteínas-G/metabolismo
Transdução de Sinais/efeitos dos fármacos
Canais de Cátion TRPV/metabolismo
Paladar
Fosfolipases Tipo C/metabolismo
[Mh] Termos MeSH secundário: Anestesia
Animais
Benzofenantridinas/farmacologia
Capsaicina/farmacologia
Cloroquina/administração & dosagem
Cloroquina/farmacologia
Estrenos/farmacologia
Infusões Intravenosas
Pirrolidinonas/farmacologia
Ratos Sprague-Dawley
Reflexo/efeitos dos fármacos
Respiração/efeitos dos fármacos
Células Receptoras Sensoriais/efeitos dos fármacos
Células Receptoras Sensoriais/metabolismo
Paladar/efeitos dos fármacos
Fosfolipases Tipo C/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzophenanthridines); 0 (Estrenes); 0 (Pyrrolidinones); 0 (Receptors, G-Protein-Coupled); 0 (TRPV Cation Channels); 0 (Trpv1 protein, rat); 0 (taste receptors, type 2); 112648-68-7 (1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione); 886U3H6UFF (Chloroquine); E3B045W6X0 (chelerythrine); EC 2.7.11.13 (Protein Kinase C); EC 3.1.4.- (Type C Phospholipases); S07O44R1ZM (Capsaicin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170612
[Lr] Data última revisão:
170612
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170108
[St] Status:MEDLINE
[do] DOI:10.1152/ajplung.00468.2016


  9 / 2830 MEDLINE  
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[PMID]:28042022
[Au] Autor:Blanco AM; Bertucci JI; Sánchez-Bretaño A; Delgado MJ; Valenciano AI; Unniappan S
[Ad] Endereço:Laboratory of Integrative Neuroendocrinology, Department of Veterinary Biomedical Sciences, Western College of Veterinary Medicine, University of Saskatchewan, 52 Campus Drive, S7N 5B4 Saskatoon, Saskatchewan, Canada; Departamento de Fisiología (Fisiología Animal II), Facultad de Biología, Universid
[Ti] Título:Ghrelin modulates gene and protein expression of digestive enzymes in the intestine and hepatopancreas of goldfish (Carassius auratus) via the GHS-R1a: Possible roles of PLC/PKC and AC/PKA intracellular signaling pathways.
[So] Source:Mol Cell Endocrinol;442:165-181, 2017 Feb 15.
[Is] ISSN:1872-8057
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Ghrelin, a multifunctional gut-brain hormone, is involved in the regulation of gastric functions in mammals. This study aimed to determine whether ghrelin modulates digestive enzymes in goldfish (Carassius auratus). Immunofluorescence microscopy found colocalization of ghrelin, GHS-R1a and the digestive enzymes sucrase-isomaltase, aminopeptidase A, trypsin and lipoprotein lipase in intestinal and hepatopancreatic cells. In vitro ghrelin treatment in intestinal and hepatopancreas explant culture led to a concentration- and time-dependent modulation (mainly stimulatory) of most of the digestive enzymes tested. The ghrelin-induced upregulations of digestive enzyme expression were all abolished by preincubation with the GHS-R1a ghrelin receptor antagonist [D-Lys3]-GHRP-6, and most of them by the phospholipase C inhibitor U73122 or the protein kinase A inhibitor H89. This indicates that ghrelin effects on digestive enzymes are mediated by GHS-R1a, partly by triggering the PLC/PKC and AC/PKA intracellular signaling pathways. These data suggest a role for ghrelin on digestive processes in fish.
[Mh] Termos MeSH primário: Grelina/farmacologia
Carpa Dourada/metabolismo
Hepatopâncreas/efeitos dos fármacos
Intestinos/efeitos dos fármacos
Receptores de Grelina/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adenilil Ciclases/metabolismo
Animais
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
Estrenos/farmacologia
Expressão Gênica/efeitos dos fármacos
Hepatopâncreas/metabolismo
Intestinos/metabolismo
Isoquinolinas/farmacologia
Fosfoinositídeo Fosfolipase C/metabolismo
Proteína Quinase C/metabolismo
Pirrolidinonas/farmacologia
Sulfonamidas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Estrenes); 0 (Ghrelin); 0 (Isoquinolines); 0 (Pyrrolidinones); 0 (Receptors, Ghrelin); 0 (Sulfonamides); 112648-68-7 (1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); EC 2.7.11.13 (Protein Kinase C); EC 3.1.4.11 (Phosphoinositide Phospholipase C); EC 4.6.1.1 (Adenylyl Cyclases); M876330O56 (N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170103
[St] Status:MEDLINE


  10 / 2830 MEDLINE  
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[PMID]:27958649
[Au] Autor:Robinson JA; Ma Q; Staveley JP; Smolenski WJ
[Ad] Endereço:Zoetis, Kalamazoo, Michigan, USA.
[Ti] Título:Sorption and desorption of 17α-trenbolone and trendione on five soils.
[So] Source:Environ Toxicol Chem;36(3):613-620, 2017 Mar.
[Is] ISSN:1552-8618
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The metabolites 17α-trenbolone and 17α-estradiol are principal metabolites in cattle excreta following the administration of Synovex ONE, which contains trenbolone acetate and estradiol benzoate. As part of the environmental assessment of the use of Synovex ONE, data were generated to characterize the fate of 17α-trenbolone, and its metabolite trendione in the environment. Predictions of the fate and environmental concentrations of these hormones after land application require accurate estimates of the sorption of these compounds in soils. The sorption and desorption of 17α-trenbolone and trendione were measured at 5 nominal concentrations in 5 soils from different geologic settings using a batch equilibrium technique following guideline 106 of the Organisation for Economic Co-operation and Development. Both the sorption and desorption of 17α-trenbolone and trendione to soils were adequately described by the Freundlich sorption model and by linear partition coefficients. The mean sorption coefficients were 9.04 mL/g and 32.2 mL/g for 17α-trenbolone and trendione, respectively. The corresponding mean Freundlich sorption exponents were 0.88 and 0.98, respectively. Sorption of 17α-trenbolone and trendione was correlated principally with soil organic carbon. Average sorption coefficients normalized to soil organic carbon content (K ) were 460 mL/g and 1804 mL/g for 17α-trenbolone and trendione, respectively. The mean desorption coefficients were 22.1 mL/g and 43.8 mL/g for 17α-trenbolone and trendione, respectively. Calculated hysteresis coefficients based on the difference in the area between sorption and desorption isotherms indicated that sorption equilibrium was not fully reversible and hysteresis of desorption isotherms occurred for both 17α-trenbolone and trendione. Environ Toxicol Chem 2017;36:613-620. © 2016 SETAC.
[Mh] Termos MeSH primário: Monitoramento Ambiental/métodos
Estrenos/química
Poluentes do Solo/química
Solo/química
Acetato de Trembolona/química
[Mh] Termos MeSH secundário: Adsorção
Animais
Bovinos
Estradiol/análogos & derivados
Estradiol/química
Estradiol/metabolismo
Estrenos/metabolismo
Fezes/química
Guias como Assunto
Cinética
Modelos Teóricos
Estrutura Molecular
Montana
North Dakota
Organização para a Cooperação e Desenvolvimento Econômico
Poluentes do Solo/metabolismo
Acetato de Trembolona/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Estrenes); 0 (Soil); 0 (Soil Pollutants); 1S4CJB5ZGN (estradiol 3-benzoate); 4642-95-9 (trendione); 4TI98Z838E (Estradiol); RUD5Y4SV0S (Trenbolone Acetate)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161214
[St] Status:MEDLINE
[do] DOI:10.1002/etc.3711



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