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  1 / 2778 MEDLINE  
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[PMID]:28475363
[Au] Autor:Srivedavyasasri R; White MB; Kustova TS; Gemejiyeva NG; Cantrell CL; Ross SA
[Ad] Endereço:a National Center for Natural Product Research , University of Mississippi , University , MS , USA.
[Ti] Título:New tetranorlabdanoic acid from aerial parts of Salvia aethiopis.
[So] Source:Nat Prod Res;32(1):14-17, 2018 Jan.
[Is] ISSN:1478-6427
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Salvia aethiopis is a perennial plant native to Eurasia and known by the common names Mediterranean sage or African sage. This plant has been used in Iranian medicine as a carminative and tonic. The ethanolic extract of aerial part of S. aethiopis exhibited moderate to weak activity towards delta and kappa opioid receptors (46.3 and 45.3% displacement, respectively). Chromatographic purification of the ethanolic extract on silica gel column led to isolation of one new: 3α-hydroxy-8α-acetoxy-13,14,15,16-tetranorlabdan-12-oic acid (I) and three known compounds: sesquiterpene spathulenol (II), ß-sitosterol (III) and ß-sitosterol-3-O-glucoside (IV). The structures of all isolated compounds were elucidated by their NMR (1D and 2D) and MS spectral data. All the fractions and isolated compounds were tested for cannabinoid and opioid receptor binding assays.
[Mh] Termos MeSH primário: Componentes Aéreos da Planta/química
Receptores de Canabinoides/metabolismo
Salvia/química
[Mh] Termos MeSH secundário: Avaliação Pré-Clínica de Medicamentos/métodos
Irã (Geográfico)
Espectroscopia de Ressonância Magnética
Estrutura Molecular
Extratos Vegetais/química
Extratos Vegetais/farmacologia
Plantas Medicinais/química
Receptores Opioides delta/metabolismo
Receptores Opioides kappa/metabolismo
Sesquiterpenos/química
Sesquiterpenos/metabolismo
Sesquiterpenos/farmacologia
Sitosteroides/química
Sitosteroides/metabolismo
Sitosteroides/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Plant Extracts); 0 (Receptors, Cannabinoid); 0 (Receptors, Opioid, delta); 0 (Receptors, Opioid, kappa); 0 (Sesquiterpenes); 0 (Sitosterols); 5LI01C78DD (gamma-sitosterol); 7XV9L96SJJ (spathulenol); U45VN859W3 (lyoniside)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170506
[St] Status:MEDLINE
[do] DOI:10.1080/14786419.2017.1324961


  2 / 2778 MEDLINE  
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[PMID]:28875496
[Au] Autor:Hasenoehrl C; Feuersinger D; Sturm EM; Bärnthaler T; Heitzer E; Graf R; Grill M; Pichler M; Beck S; Butcher L; Thomas D; Ferreirós N; Schuligoi R; Schweiger C; Haybaeck J; Schicho R
[Ad] Endereço:Institute of Experimental and Clinical Pharmacology, Medical University of Graz, Graz, Austria.
[Ti] Título:G protein-coupled receptor GPR55 promotes colorectal cancer and has opposing effects to cannabinoid receptor 1.
[So] Source:Int J Cancer;142(1):121-132, 2018 Jan 01.
[Is] ISSN:1097-0215
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The putative cannabinoid receptor GPR55 has been shown to play a tumor-promoting role in various cancers, and is involved in many physiological and pathological processes of the gastrointestinal (GI) tract. While the cannabinoid receptor 1 (CB ) has been reported to suppress intestinal tumor growth, the role of GPR55 in the development of GI cancers is unclear. We, therefore, aimed at elucidating the role of GPR55 in colorectal cancer (CRC), the third most common cancer worldwide. Using azoxymethane (AOM)- and dextran sulfate sodium (DSS)-driven CRC mouse models, we found that GPR55 plays a tumor-promoting role that involves alterations of leukocyte populations, i.e. myeloid-derived suppressor cells and T lymphocytes, within the tumor tissues. Concomitantly, expression levels of COX-2 and STAT3 were reduced in tumor tissue of GPR55 knockout mice, indicating reduced presence of tumor-promoting factors. By employing the experimental CRC models to CB knockout and CB /GPR55 double knockout mice, we can further show that GPR55 plays an opposing role to CB . We report that GPR55 and CB mRNA expression are differentially regulated in the experimental models and in a cohort of 86 CRC patients. Epigenetic methylation of CNR1 and GPR55 was also differentially regulated in human CRC tissue compared to control samples. Collectively, our data suggest that GPR55 and CB play differential roles in colon carcinogenesis where the former seems to act as oncogene and the latter as tumor suppressor.
[Mh] Termos MeSH primário: Carcinogênese/metabolismo
Neoplasias Colorretais/patologia
Receptores Acoplados a Proteínas-G/metabolismo
[Mh] Termos MeSH secundário: Animais
Neoplasias Colorretais/metabolismo
Seres Humanos
Camundongos
Camundongos Knockout
Receptor CB1 de Canabinoide/metabolismo
Receptores de Canabinoides/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GPR55 protein, human); 0 (GPR55 protein, mouse); 0 (Receptor, Cannabinoid, CB1); 0 (Receptors, Cannabinoid); 0 (Receptors, G-Protein-Coupled)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180124
[Lr] Data última revisão:
180124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170907
[St] Status:MEDLINE
[do] DOI:10.1002/ijc.31030


  3 / 2778 MEDLINE  
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[PMID]:27773824
[Au] Autor:Deng L; Lee WH; Xu Z; Makriyannis A; Hohmann AG
[Ad] Endereço:Program in Neuroscience, Department of Psychological and Brain Sciences, Indiana University, Bloomington, IN, USA; Interdisciplinary Biochemistry Graduate Program, Department of Molecular and Cellular Biochemistry, Indiana University, Bloomington, IN, USA.
[Ti] Título:Prophylactic treatment with the tricyclic antidepressant desipramine prevents development of paclitaxel-induced neuropathic pain through activation of endogenous analgesic systems.
[So] Source:Pharmacol Res;114:75-89, 2016 Dec.
[Is] ISSN:1096-1186
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Neuropathic pain impacts approximately 3-4.5% of the global population and remains an unresolved health problem. The management of neuropathic pain has two distinct goals-prevention of development and control of established neuropathic pain. We examined the impact of both prophylactic and therapeutic treatments with the tricyclic antidepressant desipramine on the development and maintenance of toxic neuropathic pain induced by the chemotherapeutic agent paclitaxel. We also investigated the involvement of endogenous analgesic (i.e., endogenous opioid and endocannabinoid) systems in the antinociceptive actions of desipramine in these two distinct phases of neuropathic pain. Chronic subcutaneous infusion of desipramine via osmotic pumps suppressed both the development and maintenance of paclitaxel-induced neuropathic pain. However, only prophylactic desipramine treatment blocked the development of neuropathic pain throughout the three month observation interval; neuropathic pain did not return. The opioid receptor antagonist naloxone blocked the antinociceptive effects of both prophylactic and therapeutic desipramine treatments throughout the entire timecourse of desipramine-induced antinociception. By contrast, cannabinoid CB and CB receptor antagonists partially attenuated the antinociceptive actions of desipramine in a manner that was restricted to the development phase of paclitaxel-induced neuropathic pain only. Paclitaxel decreased cell viability in TMD231 tumor cells in an MTT assay in vitro. Notably, desipramine (1nM-1µM) alone did not alter tumor cell viability and did not prevent the cytotoxic effects of paclitaxel under identical conditions. The highest concentration of desipramine (10µM) reduced tumor cell viability alone and enhanced the cytotoxic effects of paclitaxel. Our study identifies a previously unrecognized preemptive analgesic strategy that prevents development of paclitaxel-induced neuropathic pain, and also dissects receptor mechanisms underlying desipramine-induced antinociceptive effects. This information may be applied to improve current therapeutic strategies with the goal of preventing and managing neuropathic pain induced by chemotherapeutic treatment.
[Mh] Termos MeSH primário: Antidepressivos Tricíclicos/uso terapêutico
Antineoplásicos Fitogênicos/efeitos adversos
Desipramina/uso terapêutico
Neuralgia/induzido quimicamente
Neuralgia/prevenção & controle
Paclitaxel/efeitos adversos
[Mh] Termos MeSH secundário: Animais
Antidepressivos Tricíclicos/farmacologia
Desipramina/farmacologia
Hiperalgesia/induzido quimicamente
Hiperalgesia/prevenção & controle
Masculino
Ratos Sprague-Dawley
Receptores de Canabinoides/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antidepressive Agents, Tricyclic); 0 (Antineoplastic Agents, Phytogenic); 0 (Receptors, Cannabinoid); P88XT4IS4D (Paclitaxel); TG537D343B (Desipramine)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161107
[St] Status:MEDLINE


  4 / 2778 MEDLINE  
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[PMID]:28948607
[Au] Autor:Keresztes A; Streicher JM
[Ad] Endereço:Department of Pharmacology, College of Medicine, University of Arizona, Tucson, AZ, USA.
[Ti] Título:Synergistic interaction of the cannabinoid and death receptor systems - a potential target for future cancer therapies?
[So] Source:FEBS Lett;591(20):3235-3251, 2017 Oct.
[Is] ISSN:1873-3468
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cannabinoid receptors have been shown to interact with other receptors, including tumor necrosis factor receptor superfamily (TNFRS) members, to induce cancer cell death. When cannabinoids and death-inducing ligands (including TNF-related apoptosis-inducing ligand) are administered together, they have been shown to synergize and demonstrate enhanced antitumor activity in vitro. Certain cannabinoid ligands have been shown to sensitize cancer cells and synergistically interact with members of the TNFRS, thus suggesting that the combination of cannabinoids with death receptor (DR) ligands induces additive or synergistic tumor cell death. This review summarizes recent findings on the interaction of the cannabinoid and DR systems and suggests possible clinical co-application of cannabinoids and DR ligands in the treatment of various malignancies.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Canabinoides/uso terapêutico
Regulação Neoplásica da Expressão Gênica
Neoplasias/tratamento farmacológico
Receptores de Canabinoides/genética
Receptores de Morte Celular/genética
Ligante Indutor de Apoptose Relacionado a TNF/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Sinergismo Farmacológico
Seres Humanos
Ligantes
Neoplasias/genética
Neoplasias/metabolismo
Neoplasias/patologia
Receptor Cross-Talk
Receptores de Canabinoides/metabolismo
Receptores de Morte Celular/metabolismo
Transdução de Sinais
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cannabinoids); 0 (Ligands); 0 (Receptors, Cannabinoid); 0 (Receptors, Death Domain); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (TNFSF10 protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170927
[St] Status:MEDLINE
[do] DOI:10.1002/1873-3468.12863


  5 / 2778 MEDLINE  
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[PMID]:28782186
[Au] Autor:Sowaileh MF; Hazlitt RA; Colby DA
[Ad] Endereço:Department of BioMolecular Sciences, University of Mississippi, University, MS, 38677, USA.
[Ti] Título:Application of the Pentafluorosulfanyl Group as a Bioisosteric Replacement.
[So] Source:ChemMedChem;12(18):1481-1490, 2017 Sep 21.
[Is] ISSN:1860-7187
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The success of fluorinated molecules in drug design has led medicinal chemists to search for new fluorine-containing substituents. A major recently developed group is the pentafluorosulfanyl group. This group is stable under physiological conditions and displays unique physical and chemical properties. There are currently few synthetic methods to install the SF group, yet efforts to integrate this group into lead optimization continue unabated. Typically, the SF group has been used as a replacement for trifluoromethyl, tert-butyl, halogen, or nitro groups. In this review, the use of the SF group as a bioisosteric replacement for each of these three functionalities is compared and contrasted across various groups of biologically active molecules. The organization and presentation of these data should be instructive to medicinal chemists considering to design synthetic strategies to access SF -substituted molecules.
[Mh] Termos MeSH primário: Sulfetos/química
Compostos de Enxofre/química
[Mh] Termos MeSH secundário: Antiprotozoários/química
Antiprotozoários/farmacologia
Desenho de Drogas
Ácido Flufenâmico/análogos & derivados
Ácido Flufenâmico/farmacologia
Halogenação
NADH NADPH Oxirredutases/antagonistas & inibidores
NADH NADPH Oxirredutases/metabolismo
Oxirredutases atuantes sobre Doadores de Grupo CH-CH/antagonistas & inibidores
Oxirredutases atuantes sobre Doadores de Grupo CH-CH/metabolismo
Plasmodium falciparum/efeitos dos fármacos
Plasmodium falciparum/enzimologia
Ligação Proteica
Receptores de Canabinoides/química
Receptores de Canabinoides/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antiprotozoal Agents); 0 (Receptors, Cannabinoid); 0 (Sulfides); 0 (Sulfur Compounds); 60GCX7Y6BH (Flufenamic Acid); EC 1.3.- (Oxidoreductases Acting on CH-CH Group Donors); EC 1.3.5.2 (dihydroorotate dehydrogenase); EC 1.6.- (NADH, NADPH Oxidoreductases); EC 1.8.1.12 (trypanothione reductase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170808
[St] Status:MEDLINE
[do] DOI:10.1002/cmdc.201700356


  6 / 2778 MEDLINE  
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[PMID]:28726104
[Au] Autor:Akimov MG; Ashba AM; Gretskaya NM; Bezuglov VV
[Ad] Endereço:Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, Moscow, 117997, Russia. akimovmike@yandex.ru.
[Ti] Título:N-acyl dopamines induce apoptosis in PC12 cell line via the GPR55 receptor activation.
[So] Source:Dokl Biochem Biophys;474(1):155-158, 2017 May.
[Is] ISSN:1608-3091
[Cp] País de publicação:Russia (Federation)
[La] Idioma:eng
[Ab] Resumo:Dopamine amides of arachidonic, docosahexaenoic, and oleic acids were found to induce apoptosis in PC12 cells, which was blocked exclusively by antagonists and preincubation agonists of the receptor GPR55, belonging to the group of non-CB1/CB2 receptors.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Dopamina/química
Dopamina/farmacologia
Receptores de Canabinoides/metabolismo
Receptores Acoplados a Proteínas-G/metabolismo
[Mh] Termos MeSH secundário: Animais
Cinética
Células PC12
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GPR55 protein, rat); 0 (Receptors, Cannabinoid); 0 (Receptors, G-Protein-Coupled); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE
[do] DOI:10.1134/S1607672917030012


  7 / 2778 MEDLINE  
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[PMID]:28655715
[Au] Autor:Chia CW; Carlson OD; Liu DD; González-Mariscal I; Santa-Cruz Calvo S; Egan JM
[Ad] Endereço:Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, Maryland chiac@mail.nih.gov.
[Ti] Título:Incretin secretion in humans is under the influence of cannabinoid receptors.
[So] Source:Am J Physiol Endocrinol Metab;313(3):E359-E366, 2017 Sep 01.
[Is] ISSN:1522-1555
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The mechanisms regulating incretin secretion are not fully known. Human obesity is associated with altered incretin secretion and elevated endocannabinoid levels. Since cannabinoid receptors (CBRs) are expressed on incretin-secreting cells in rodents, we hypothesized that endocannabinoids are involved in the regulation of incretin secretion. We compared plasma glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) responses during oral glucose tolerance test (OGTT) in 20 lean and 20 obese participants from the Baltimore Longitudinal Study of Aging (BLSA). Next, we recruited 20 healthy men to evaluate GIP and GLP-1 responses during OGTT after administering placebo or nabilone (CBR agonist) in a randomized, double-blind, crossover fashion. Compared with the BLSA lean group, the BLSA obese group had significantly higher fasting and post-OGTT GIP levels, but similar fasting GLP-1 and significantly lower post-OGTT GLP-1 levels. In the nabilone vs. placebo study, when compared with placebo, nabilone resulted in significantly elevated post-dose fasting GIP levels and post-OGTT GIP levels, but no change in post-dose fasting GLP-1 levels together with significantly lower post-OGTT GLP-1 levels. Glucose levels were not different with both interventions. We conclude that elevated GIP levels in obesity are likely a consequence of increased endocannabinoid levels. CBRs exert tonic control over GIP secretion, which may have a homeostatic effect in suppressing GLP-1 secretion. This raises the possibility that gut hormones are influenced by endocannabinoids.
[Mh] Termos MeSH primário: Agonistas de Receptores de Canabinoides/farmacologia
Dronabinol/análogos & derivados
Polipeptídeo Inibidor Gástrico/efeitos dos fármacos
Peptídeo 1 Semelhante ao Glucagon/efeitos dos fármacos
Obesidade/metabolismo
Receptores de Canabinoides/metabolismo
[Mh] Termos MeSH secundário: Adulto
Glicemia/metabolismo
Estudos de Casos e Controles
Estudos Cross-Over
Método Duplo-Cego
Dronabinol/farmacologia
Feminino
Polipeptídeo Inibidor Gástrico/sangue
Polipeptídeo Inibidor Gástrico/secreção
Peptídeo 1 Semelhante ao Glucagon/sangue
Peptídeo 1 Semelhante ao Glucagon/secreção
Teste de Tolerância a Glucose
Seres Humanos
Incretinas/sangue
Incretinas/secreção
Estudos Longitudinais
Masculino
Meia-Idade
Estudos Prospectivos
Receptores de Canabinoides/efeitos dos fármacos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Cannabinoid Receptor Agonists); 0 (Incretins); 0 (Receptors, Cannabinoid); 2N4O9L084N (nabilone); 59392-49-3 (Gastric Inhibitory Polypeptide); 7J8897W37S (Dronabinol); 89750-14-1 (Glucagon-Like Peptide 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170629
[St] Status:MEDLINE
[do] DOI:10.1152/ajpendo.00080.2017


  8 / 2778 MEDLINE  
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[PMID]:28608560
[Au] Autor:Basavarajappa BS; Shivakumar M; Joshi V; Subbanna S
[Ad] Endereço:Division of Analytical Psychopharmacology, Nathan Kline Institute for Psychiatric Research, Orangeburg, New York, USA.
[Ti] Título:Endocannabinoid system in neurodegenerative disorders.
[So] Source:J Neurochem;142(5):624-648, 2017 Sep.
[Is] ISSN:1471-4159
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Most neurodegenerative disorders (NDDs) are characterized by cognitive impairment and other neurological defects. The definite cause of and pathways underlying the progression of these NDDs are not well-defined. Several mechanisms have been proposed to contribute to the development of NDDs. These mechanisms may proceed concurrently or successively, and they differ among cell types at different developmental stages in distinct brain regions. The endocannabinoid system, which involves cannabinoid receptors type 1 (CB1R) and type 2 (CB2R), endogenous cannabinoids and the enzymes that catabolize these compounds, has been shown to contribute to the development of NDDs in several animal models and human studies. In this review, we discuss the functions of the endocannabinoid system in NDDs and converse the therapeutic efficacy of targeting the endocannabinoid system to rescue NDDs.
[Mh] Termos MeSH primário: Moduladores de Receptores de Canabinoides/metabolismo
Endocanabinoides/metabolismo
Doenças Neurodegenerativas/tratamento farmacológico
Doenças Neurodegenerativas/metabolismo
[Mh] Termos MeSH secundário: Animais
Moduladores de Receptores de Canabinoides/uso terapêutico
Endocanabinoides/uso terapêutico
Seres Humanos
Receptores de Canabinoides/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cannabinoid Receptor Modulators); 0 (Endocannabinoids); 0 (Receptors, Cannabinoid)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171105
[Lr] Data última revisão:
171105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170614
[St] Status:MEDLINE
[do] DOI:10.1111/jnc.14098


  9 / 2778 MEDLINE  
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[PMID]:28578322
[Au] Autor:Chang X; Bian Y; He Q; Yao J; Zhu J; Wu J; Wang K; Duan T
[Ad] Endereço:Clinical and Translational Research Center, Shanghai, China.
[Ti] Título:Suppression of STAT3 Signaling by Δ9-Tetrahydrocannabinol (THC) Induces Trophoblast Dysfunction.
[So] Source:Cell Physiol Biochem;42(2):537-550, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:AIMS: Marijuana is a widely used illicit drug and its consumption during pregnancy has been associated with adverse reproductive outcomes. The purpose of this study was to determine the effects of chronic intake of Δ9-tetrahydrocannabinol (THC), the major component of marijuana, on trophoblast function, placental development, and birth outcomes. METHODS: The pathological characteristics and distribution of cannabinoid receptors in placenta were observed by immunohistochemical (IHC) staining. Cell migration in response to THC was measured by transwell assays. The levels of cannabinoid receptors and Signal Transducer and Activator of Transcription 3 (STAT3) were detected by western blot. RESULTS: We found the placenta expressed two main cannabinoid receptors, suggesting that THC induced biological responses in placental cells. Supporting this hypothesis, we observed dramatic alterations of placental morphology in marijuana users. Using THC and inhibitors of cannabinoid receptors, we demonstrated that THC impaired trophoblast cell migration and invasion partly via cannabinoid receptors. Additionally, pregnant mice injected with THC showed adverse reproductive events including reduced number of fetuses, lower maternal and placental weights. Mechanistically, STAT3 signaling pathway was involved in the THC-induced suppression of trophoblast cell motility and pregnancy outcomes. CONCLUSION: Our study indicates that the STAT3 signaling pathway plays a critical role in THC-induced trophoblast dysfunction.
[Mh] Termos MeSH primário: Cannabis/efeitos adversos
Dronabinol/efeitos adversos
Abuso de Maconha/genética
Fator de Transcrição STAT3/genética
[Mh] Termos MeSH secundário: Adulto
Animais
Coeficiente de Natalidade
Canabinoides/efeitos adversos
Feminino
Seres Humanos
Abuso de Maconha/patologia
Camundongos
Placenta/efeitos dos fármacos
Placenta/patologia
Gravidez
Receptores de Canabinoides/biossíntese
Receptores de Canabinoides/genética
Fator de Transcrição STAT3/biossíntese
Transdução de Sinais/efeitos dos fármacos
Trofoblastos/efeitos dos fármacos
Trofoblastos/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cannabinoids); 0 (Receptors, Cannabinoid); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 7J8897W37S (Dronabinol)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170804
[Lr] Data última revisão:
170804
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170605
[St] Status:MEDLINE
[do] DOI:10.1159/000477603


  10 / 2778 MEDLINE  
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[PMID]:28533434
[Au] Autor:Harada K; Kitaguchi T; Kamiya T; Aung KH; Nakamura K; Ohta K; Tsuboi T
[Ad] Endereço:From the Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, Tokyo 153-8902, Japan.
[Ti] Título:Lysophosphatidylinositol-induced activation of the cation channel TRPV2 triggers glucagon-like peptide-1 secretion in enteroendocrine L cells.
[So] Source:J Biol Chem;292(26):10855-10864, 2017 Jun 30.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The lysophosphatidylinositol (LPI) has crucial roles in multiple physiological processes, including insulin exocytosis from pancreatic islets. However, the role of LPI in secretion of glucagon-like peptide-1 (GLP-1), a hormone that enhances glucose-induced insulin secretion, is unclear. Here, we used the murine enteroendocrine L cell line GLUTag and primary murine small intestinal cells to elucidate the mechanism of LPI-induced GLP-1 secretion. Exogenous LPI addition increased intracellular Ca concentrations ([Ca ] ) in GLUTag cells and induced GLP-1 secretion from both GLUTag and acutely prepared primary intestinal cells. The [Ca ] increase was suppressed by an antagonist for G protein-coupled receptor 55 (GPR55) and by silencing of GPR55 expression, indicating involvement of G and G signaling pathways in the LPI-induced increased [Ca ] levels and GLP-1 secretion. However, GPR55 agonists did not mimic many of the effects of LPI. We also found that phospholipase C inhibitor and Rho-associated kinase inhibitor suppressed the [Ca ] increase and that LPI increased the number of focal adhesions, indicating actin reorganization. Of note, blockage or silencing of transient receptor potential cation channel subfamily V member 2 (TRPV2) channels suppressed both the LPI-induced [Ca ] increase and GLP-1 secretion. Furthermore, LPI accelerated TRPV2 translocation to the plasma membrane, which was significantly suppressed by a GPR55 antagonist. These findings suggest that TRPV2 activation via actin reorganization induced by G and G signaling is involved in LPI-stimulated GLP-1 secretion in enteroendocrine L cells. Because GPR55 agonists largely failed to mimic the effects of LPI, its actions on L cells are at least partially independent of GPR55 activation.
[Mh] Termos MeSH primário: Canais de Cálcio/metabolismo
Sinalização do Cálcio/fisiologia
Células Enteroendócrinas/metabolismo
Peptídeo 1 Semelhante ao Glucagon/secreção
Lisofosfolipídeos/metabolismo
Canais de Cátion TRPV/metabolismo
[Mh] Termos MeSH secundário: Animais
Canais de Cálcio/genética
Células Cultivadas
Adesões Focais/genética
Adesões Focais/metabolismo
Subunidades alfa de Proteínas de Ligação ao GTP/genética
Subunidades alfa de Proteínas de Ligação ao GTP/metabolismo
Peptídeo 1 Semelhante ao Glucagon/genética
Camundongos
Transporte Proteico/fisiologia
Receptores de Canabinoides/genética
Receptores de Canabinoides/metabolismo
Canais de Cátion TRPV/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channels); 0 (GPR55 protein, mouse); 0 (GTP-Binding Protein alpha Subunits); 0 (Lysophospholipids); 0 (Receptors, Cannabinoid); 0 (TRPV Cation Channels); 0 (Trpv2 protein, mouse); 0 (lysophosphatidylinositol); 89750-14-1 (Glucagon-Like Peptide 1)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170714
[Lr] Data última revisão:
170714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170524
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.788653



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