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[PMID]:28460633
[Au] Autor:Zhang Z; Zheng W; Xie H; Chai R; Wang J; Zhang H; He S
[Ad] Endereço:Allergy and Clinical Immunology Research Centre, The First Affiliated Hospital of Jinzhou Medical University, No. 2, Section 5, Renmin Street, Guta District, Jinzhou, 121001, Liaoning, People's Republic of China.
[Ti] Título:Up-regulated expression of substance P in CD8 T cells and NK1R on monocytes of atopic dermatitis.
[So] Source:J Transl Med;15(1):93, 2017 May 01.
[Is] ISSN:1479-5876
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Large numbers of CD8 T cells were observed in atopic dermatitis (AD) skin, and monocytes from AD patients showed increased prostaglandin E2 production. However, little is known about the expression of substance P (SP) and its receptor NK1R in blood leukocytes of patients with AD. OBJECTIVE: To explore the expression of SP and NK1R in leukocytes of AD and the influence of allergens on SP and NK1R expression. METHODS: The expression levels of SP and NK1R in patients with AD were examined by flow cytometry, ELISA and a mouse AD model. RESULTS: The plasma SP level was 4.9-fold higher in patients with AD than in HC subjects. Both the percentage of SP expression in the population and mean fluorescence intensity (MFI) of SP expression were elevated in CD8 T cells in the blood of AD patients. However, both the CD14 NK1R population and MFI of NK1R expression on CD14 cells were enhanced in the blood of AD patients. Allergens ASWE, HDME and PPE failed to up-regulate SP expression in CD8 T cells. However, allergens ASWE and HDME both enhanced NK1R expression on CD14 blood leukocytes regardless of AD or HC subjects. OVA-sensitized AD mice showed an elevated proportion and MFI of SP-expressing CD8 T cells in the blood, which agrees with the SP expression situation in human AD blood. Injection of SP into mouse skin did not up-regulate NK1R expression on monocytes. CONCLUSIONS: An elevated plasma SP level, up-regulated expression of SP and NK1R indicate that the SP/NK1R complex is important in the development of AD. Therefore, SP and NK1R antagonist or blocker agents may help to treat patients with AD. Trial registration Registration number: ChiCTR-BOC-16010279; Registration date: Dec., 28, 2016; retrospectively registered.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/imunologia
Dermatite Atópica/genética
Dermatite Atópica/imunologia
Monócitos/patologia
Receptores da Neurocinina-1/metabolismo
Substância P/genética
Regulação para Cima/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Alérgenos/imunologia
Animais
Estudos de Casos e Controles
Dermatite Atópica/sangue
Citometria de Fluxo
Seres Humanos
Camundongos Endogâmicos BALB C
Meia-Idade
Ovalbumina/imunologia
Substância P/sangue
Substância P/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Allergens); 0 (Receptors, Neurokinin-1); 33507-63-0 (Substance P); 9006-59-1 (Ovalbumin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1186/s12967-017-1196-6


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[PMID]:27773805
[Au] Autor:Camilleri M; Sellin JH; Barrett KE
[Ad] Endereço:Clinical Enteric Neuroscience Translational and Epidemiological Research, Division of Gastroenterology and Hepatology, Department of Medicine, Mayo Clinic, Rochester, Minnesota. Electronic address: camilleri.michael@mayo.edu.
[Ti] Título:Pathophysiology, Evaluation, and Management of Chronic Watery Diarrhea.
[So] Source:Gastroenterology;152(3):515-532.e2, 2017 Feb.
[Is] ISSN:1528-0012
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chronic watery diarrhea poses a diagnostic and therapeutic challenge and is often a disabling condition for patients. Although acute diarrhea is likely to be caused by infection, the causes of chronic diarrhea (>4 weeks in duration) are more elusive. We review the pathophysiology, diagnosis, and treatment of chronic diarrhea. Drawing on recent insights into the molecular mechanisms of intestinal epithelial transport and barrier function, we discuss how diarrhea can result from a decrease in luminal solute absorption, an increase in secretion, or both, as well as derangements in barrier properties. We also describe the various extraepithelial factors that activate diarrheal mechanisms. Finally, clinical evaluation and tests used in the assessment of patients presenting with chronic diarrhea are reviewed, and an algorithm guiding therapeutic decisions and pharmacotherapy is presented.
[Mh] Termos MeSH primário: Diarreia/metabolismo
Absorção Intestinal
Secreções Intestinais
Intestinos/metabolismo
[Mh] Termos MeSH secundário: Proteína C-Reativa/metabolismo
Cromograninas/metabolismo
Doença Crônica
Diarreia/diagnóstico
Diarreia/fisiopatologia
Diarreia/terapia
Fezes/química
Motilidade Gastrointestinal
Seres Humanos
Inflamação
Intestinos/fisiopatologia
Síndrome do Intestino Irritável/metabolismo
Lactoferrina/metabolismo
Complexo Antígeno L1 Leucocitário/metabolismo
Concentração Osmolar
Permeabilidade
Prostaglandinas/metabolismo
Serotonina/metabolismo
Substância P/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Chromogranins); 0 (Leukocyte L1 Antigen Complex); 0 (Prostaglandins); 333DO1RDJY (Serotonin); 33507-63-0 (Substance P); 9007-41-4 (C-Reactive Protein); EC 3.4.21.- (Lactoferrin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180201
[Lr] Data última revisão:
180201
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:29281692
[Au] Autor:Hertler B; Hosp JA; Blanco MB; Luft AR
[Ad] Endereço:Division of Vascular Neurology and Rehabilitation, Department of Neurology, University and University Hospital of Zurich, Zurich, Switzerland.
[Ti] Título:Substance P signalling in primary motor cortex facilitates motor learning in rats.
[So] Source:PLoS One;12(12):e0189812, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Among the genes that are up-regulated in response to a reaching training in rats, Tachykinin 1 (Tac1)-a gene that encodes the neuropeptide Substance P (Sub P)-shows an especially strong expression. Using Real-Time RT-PCR, a detailed time-course of Tac1 expression could be defined: a significant peak occurs 7 hours after training ended at the first and second training session, whereas no up-regulation could be detected at a later time-point (sixth training session). To assess the physiological role of Sub P during movement acquisition, microinjections into the primary motor cortex (M1) contralateral to the trained paw were performed. When Sub P was injected before the first three sessions of a reaching training, effectiveness of motor learning became significantly increased. Injections at a time-point when rats already knew the task (i.e. training session ten and eleven) had no effect on reaching performance. Sub P injections did not influence the improvement of performance within a single training session, but retention of performance between sessions became strengthened at a very early stage (i.e. between baseline-training and first training session). Thus, Sub P facilitates motor learning in the very early phase of skill acquisition by supporting memory consolidation. In line with these findings, learning related expression of the precursor Tac1 occurs at early but not at later time-points during reaching training.
[Mh] Termos MeSH primário: Aprendizagem
Córtex Motor/metabolismo
Destreza Motora
Transdução de Sinais
Substância P/metabolismo
[Mh] Termos MeSH secundário: Animais
Masculino
Ratos
Ratos Long-Evans
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
33507-63-0 (Substance P)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171228
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189812


  4 / 16339 MEDLINE  
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[PMID]:28452955
[Au] Autor:Grässel S; Muschter D
[Ad] Endereço:Department of Orthopedic Surgery, Exp. Orthopedics, ZMB/Biopark 1, University of Regensburg, 93053 Regensburg, Germany. susanne.graessel@ukr.de.
[Ti] Título:Peripheral Nerve Fibers and Their Neurotransmitters in Osteoarthritis Pathology.
[So] Source:Int J Mol Sci;18(5), 2017 Apr 28.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The importance of the nociceptive nervous system for maintaining tissue homeostasis has been known for some time, and it has also been suggested that organogenesis and tissue repair are under neuronal control. Changes in peripheral joint innervation are supposed to be partly responsible for degenerative alterations in joint tissues which contribute to development of osteoarthritis. Various resident cell types of the musculoskeletal system express receptors for sensory and sympathetic neurotransmitters, allowing response to peripheral neuronal stimuli. Among them are mesenchymal stem cells, synovial fibroblasts, bone cells and chondrocytes of different origin, which express distinct subtypes of adrenoceptors (AR), receptors for vasoactive intestinal peptide (VIP), substance P (SP) and calcitonin gene-related peptide (CGRP). Some of these cell types synthesize and secrete neuropeptides such as SP, and they are positive for tyrosine-hydroxylase (TH), the rate limiting enzyme for biosynthesis of catecholamines. Sensory and sympathetic neurotransmitters are involved in the pathology of inflammatory diseases such as rheumatoid arthritis (RA) which manifests mainly in the joints. In addition, they seem to play a role in pathogenesis of priori degenerative joint disorders such as osteoarthritis (OA). Altogether it is evident that sensory and sympathetic neurotransmitters have crucial trophic effects which are critical for joint tissue and bone homeostasis. They modulate articular cartilage, subchondral bone and synovial tissue properties in physiological and pathophysiological conditions, in addition to their classical neurological features.
[Mh] Termos MeSH primário: Neurotransmissores/metabolismo
Osteoartrite/patologia
Nervos Periféricos/metabolismo
[Mh] Termos MeSH secundário: Peptídeo Relacionado com Gene de Calcitonina/metabolismo
Condrócitos/citologia
Condrócitos/metabolismo
Seres Humanos
Neuropeptídeos/metabolismo
Osteoartrite/metabolismo
Receptores Adrenérgicos/metabolismo
Substância P/metabolismo
Peptídeo Intestinal Vasoativo/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Neuropeptides); 0 (Neurotransmitter Agents); 0 (Receptors, Adrenergic); 33507-63-0 (Substance P); 37221-79-7 (Vasoactive Intestinal Peptide); 83652-28-2 (Calcitonin Gene-Related Peptide)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180122
[Lr] Data última revisão:
180122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE


  5 / 16339 MEDLINE  
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[PMID]:28977601
[Au] Autor:Garcia JP; Guerriero KA; Keen KL; Kenealy BP; Seminara SB; Terasawa E
[Ad] Endereço:Wisconsin National Primate Research Center, Madison, Wisconsin 53715.
[Ti] Título:Kisspeptin and Neurokinin B Signaling Network Underlies the Pubertal Increase in GnRH Release in Female Rhesus Monkeys.
[So] Source:Endocrinology;158(10):3269-3280, 2017 Oct 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Loss-of-function or inactivating mutations in the genes coding for kisspeptin and its receptor (KISS1R) or neurokinin B (NKB) and the NKB receptor (NK3R) in humans result in a delay in or the absence of puberty. However, precise mechanisms of kisspeptin and NKB signaling in the regulation of the pubertal increase in gonadotropin-releasing hormone (GnRH) release in primates are unknown. In this study, we conducted a series of experiments infusing agonists and antagonists of kisspeptin and NKB into the stalk-median eminence, where GnRH, kisspeptin, and NKB neuroterminal fibers are concentrated, and measuring GnRH release in prepubertal and pubertal female rhesus monkeys. Results indicate that (1) similar to those previously reported for GnRH stimulation by the KISS1R agonist (i.e., human kisspeptin-10), the NK3R agonist senktide stimulated GnRH release in a dose-responsive manner in both prepubertal and pubertal monkeys; (2) the senktide-induced GnRH release was blocked in the presence of the KISS1R antagonist peptide 234 in pubertal but not prepubertal monkeys; and (3) the kisspeptin-induced GnRH release was blocked in the presence of the NK3R antagonist SB222200 in the pubertal but not prepubertal monkeys. These results are interpreted to mean that although, in prepubertal female monkeys, kisspeptin and NKB signaling to GnRH release is independent, in pubertal female monkeys, a reciprocal signaling mechanism between kisspeptin and NKB neurons is established. We speculate that this cooperative mechanism by the kisspeptin and NKB network underlies the pubertal increase in GnRH release in female monkeys.
[Mh] Termos MeSH primário: Hormônio Liberador de Gonadotropina/secreção
Kisspeptinas/fisiologia
Macaca mulatta/fisiologia
Neurocinina B/fisiologia
Maturidade Sexual/fisiologia
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Animais
Feminino
Kisspeptinas/agonistas
Kisspeptinas/antagonistas & inibidores
Kisspeptinas/farmacologia
Eminência Mediana/efeitos dos fármacos
Neurocinina B/agonistas
Neurocinina B/antagonistas & inibidores
Neurônios/metabolismo
Fragmentos de Peptídeos/farmacologia
Quinolinas/farmacologia
Receptores Acoplados a Proteínas-G/agonistas
Receptores Acoplados a Proteínas-G/antagonistas & inibidores
Receptores de Kisspeptina-1
Receptores da Neurocinina-3/agonistas
Transdução de Sinais/efeitos dos fármacos
Substância P/análogos & derivados
Substância P/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (KISS1 protein, human); 0 (KISS1R protein, human); 0 (Kisspeptins); 0 (Peptide Fragments); 0 (Quinolines); 0 (Receptors, G-Protein-Coupled); 0 (Receptors, Kisspeptin-1); 0 (Receptors, Neurokinin-3); 0 (SB 222200); 106128-89-6 (senktide); 33507-63-0 (Substance P); 33515-09-2 (Gonadotropin-Releasing Hormone); 86933-75-7 (Neurokinin B)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171005
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00500


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[PMID]:28931039
[Au] Autor:Bright FM; Vink R; Byard RW; Duncan JR; Krous HF; Paterson DS
[Ad] Endereço:Discipline of Anatomy and Pathology, Adelaide Medical School, University of Adelaide, Adelaide, SA, Australia.
[Ti] Título:Abnormalities in substance P neurokinin-1 receptor binding in key brainstem nuclei in sudden infant death syndrome related to prematurity and sex.
[So] Source:PLoS One;12(9):e0184958, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sudden infant death syndrome (SIDS) involves failure of arousal to potentially life threatening events, including hypoxia, during sleep. While neuronal dysfunction and abnormalities in neurotransmitter systems within the medulla oblongata have been implicated, the specific pathways associated with autonomic and cardiorespiratory failure are unknown. The neuropeptide substance P (SP) and its tachykinin neurokinin-1 receptor (NK1R) have been shown to play an integral role in the modulation of homeostatic function in the medulla, including regulation of respiratory rhythm generation, integration of cardiovascular control, and modulation of the baroreceptor reflex and mediation of the chemoreceptor reflex in response to hypoxia. Abnormalities in SP neurotransmission may therefore result in autonomic dysfunction during sleep and contribute to SIDS deaths. [125I] Bolton Hunter SP autoradiography was used to map the distribution and density of the SP, NK1R to 13 specific nuclei intimately related to cardiorespiratory function and autonomic control in the human infant medulla of 55 SIDS and 21 control (non-SIDS) infants. Compared to controls, SIDS cases exhibited a differential, abnormal developmental profile of the SP/NK1R system in the medulla. Furthermore the study revealed significantly decreased NK1R binding within key medullary nuclei in SIDS cases, principally in the nucleus tractus solitarii (NTS) and all three subdivisions of the inferior portion of the olivo-cerebellar complex; the principal inferior olivary complex (PIO), medial accessory olive (MAO) and dorsal accessory olive (DAO). Altered NK1R binding was significantly influenced by prematurity and male sex, which may explain the increased risk of SIDS in premature and male infants. Abnormal NK1R binding in these medullary nuclei may contribute to the defective interaction of critical medullary mechanisms with cerebellar sites, resulting in an inability of a SIDS infant to illicit appropriate respiratory and motor responses to life threatening challenges during sleep. These observations support the concept that abnormalities in a multi-neurotransmitter network within key nuclei of the medullary homeostatic system may underlie the pathogenesis of a subset of SIDS cases.
[Mh] Termos MeSH primário: Tronco Encefálico/patologia
Recém-Nascido Prematuro/metabolismo
Bulbo/patologia
Núcleo Olivar/patologia
Receptores da Neurocinina-1/metabolismo
Substância P/metabolismo
Morte Súbita do Lactente/patologia
[Mh] Termos MeSH secundário: Tronco Encefálico/metabolismo
Estudos de Coortes
Feminino
Seres Humanos
Lactente
Recém-Nascido
Masculino
Bulbo/metabolismo
Núcleo Olivar/metabolismo
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Neurokinin-1); 33507-63-0 (Substance P)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184958


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[PMID]:28827386
[Au] Autor:Suvas S
[Ad] Endereço:Department of Ophthalmology/Kresge Eye Institute, Wayne State University School of Medicine, Detroit, MI 48201; ssuvas@med.wayne.edu.
[Ti] Título:Role of Substance P Neuropeptide in Inflammation, Wound Healing, and Tissue Homeostasis.
[So] Source:J Immunol;199(5):1543-1552, 2017 Sep 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Substance P (SP) is an undecapeptide present in the CNS and the peripheral nervous system. SP released from the peripheral nerves exerts its biological and immunological activity via high-affinity neurokinin 1 receptor (NK1R). SP is also produced by immune cells and acts as an autocrine or paracrine fashion to regulate the function of immune cells. In addition to its proinflammatory role, SP and its metabolites in combination with insulin-like growth factor-1 are shown to promote the corneal epithelial wound healing. Recently, we showed an altered ocular surface homeostasis in unmanipulated NK1R mice, suggesting the role of SP-NK1R signaling in ocular surface homeostasis under steady-state. This review summarizes the immunobiology of SP and its effect on immune cells and immunity to microbial infection. In addition, the effect of SP in inflammation, wound healing, and corneal epithelial homeostasis in the eye is discussed.
[Mh] Termos MeSH primário: Inflamação/imunologia
Sistema Nervoso
Neuroimunomodulação
Neurotransmissores/imunologia
Substância P/imunologia
[Mh] Termos MeSH secundário: Animais
Córnea/metabolismo
Córnea/patologia
Homeostase
Seres Humanos
Fator de Crescimento Insulin-Like I/análogos & derivados
Fator de Crescimento Insulin-Like I/metabolismo
Camundongos
Receptores da Neurocinina-1/genética
Receptores da Neurocinina-1/metabolismo
Transdução de Sinais
Cicatrização
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Neurotransmitter Agents); 0 (Receptors, Neurokinin-1); 0 (insulin-like growth factor-1 D peptide); 33507-63-0 (Substance P); 67763-96-6 (Insulin-Like Growth Factor I)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171028
[Lr] Data última revisão:
171028
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170823
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601751


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[PMID]:28827027
[Au] Autor:Priyadarsini S; Rowsey TG; Ma JX; Karamichos D
[Ad] Endereço:Department of Ophthalmology, Dean McGee Eye Institute, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
[Ti] Título:Unravelling the stromal-nerve interactions in the human diabetic cornea.
[So] Source:Exp Eye Res;164:22-30, 2017 Nov.
[Is] ISSN:1096-0007
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Corneal defects due to diabetes mellitus (DM) may cause severe vision impairments. Current studies focus on the corneal epithelium and nerve defects neglecting the corneal stroma. The aim of this study was to develop a 3D in vitro model to examine the interactions between corneal stroma and nerves in the context of DM. Primary human corneal stromal fibroblasts isolated from healthy (HCFs), Type 1 (T1DM) and Type 2 (T2DM) patients were stimulated with stable ascorbic acid to secrete and assemble an extracellular matrix (ECM). Human neuronal cells were then seeded on top and differentiated to create the 3D co-cultures. Our data revealed successful co-culture of stromal fibroblasts and neuronal cells with large elongated neuron extensions. T2DM showed significant upregulation of Collagen III and IGF1 when compared to T1DM. Interestingly, upon nerve addition, those markers returned to HCF levels. Neuronal markers were also differentially modulated with T2DM co-cultures expressing high levels of ßIII tubulin where T1DM co-cultures expressed Substance P. . Overall, our unique 3D co-culture model provides us with a tool that can be utilized for both molecular and therapeutic studies for diabetic keratopathy.
[Mh] Termos MeSH primário: Doenças da Córnea/patologia
Substância Própria/inervação
Retinopatia Diabética/metabolismo
Retinopatia Diabética/patologia
[Mh] Termos MeSH secundário: Biomarcadores/metabolismo
Estudos de Casos e Controles
Diferenciação Celular
Células Cultivadas
Técnicas de Cocultura
Colágeno/metabolismo
Doenças da Córnea/metabolismo
Diabetes Mellitus Tipo 1/complicações
Diabetes Mellitus Tipo 2/complicações
Matriz Extracelular/metabolismo
Feminino
Fibroblastos/metabolismo
Seres Humanos
Fator de Crescimento Insulin-Like I/metabolismo
Masculino
Meia-Idade
Modelos Biológicos
Neurônios/metabolismo
Receptor IGF Tipo 1/metabolismo
Substância P/metabolismo
Tubulina (Proteína)/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Tubulin); 33507-63-0 (Substance P); 67763-96-6 (Insulin-Like Growth Factor I); 9007-34-5 (Collagen); EC 2.7.10.1 (Receptor, IGF Type 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170823
[St] Status:MEDLINE


  9 / 16339 MEDLINE  
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[PMID]:28754588
[Au] Autor:Jung N; Um J; Kim DY; Dubon MJ; Byeon Y; Kim D; Son Y; Park KS
[Ad] Endereço:Graduate School of Biotechnology, Kyung Hee University, Yong in, 17104, South Korea.
[Ti] Título:Substance P preserves pancreatic ß-cells in streptozotocin-induced type 1 diabetic mice.
[So] Source:Biochem Biophys Res Commun;491(4):958-965, 2017 Sep 30.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Preservation of the pancreatic ß-cell population is required for the development of therapies for diabetes, which is caused by a decrease in ß-cells. Here, we demonstrate the antidiabetic effects of substance P (SP) in type 1 diabetes (T1D) mice induced with streptozotocin. SP enhanced the compensatory proliferation of ß-cells in order to restore ß-cells in response to acute injury induced by a single high-dose of streptozotocin. However, SP affected neither the basal proliferation of ß-cells nor their apoptosis. In vitro studies by using the INS-1 pancreatic ß-cell line showed that SP mediated the increase in the proliferation of ß-cells via the activation of Akt. Chronic systemic treatment with SP restored the mass of ß-cells and inhibited insulitis in T1D mice induced with multiple low-doses of streptozotocin. Therefore, systemic treatment with SP may be a promising therapeutic strategy for treating diabetes in patients with loss of functional ß-cells.
[Mh] Termos MeSH primário: Diabetes Mellitus Experimental/prevenção & controle
Diabetes Mellitus Tipo 1/prevenção & controle
Células Secretoras de Insulina/efeitos dos fármacos
Pancreatite/prevenção & controle
Substância P/farmacologia
[Mh] Termos MeSH secundário: Doença Aguda
Animais
Apoptose/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Diabetes Mellitus Experimental/induzido quimicamente
Diabetes Mellitus Experimental/patologia
Diabetes Mellitus Tipo 1/induzido quimicamente
Diabetes Mellitus Tipo 1/patologia
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Injeções Intraperitoneais
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Endogâmicos ICR
Pancreatite/induzido quimicamente
Pancreatite/patologia
Estreptozocina/administração & dosagem
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
33507-63-0 (Substance P); 5W494URQ81 (Streptozocin)
[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:170730
[St] Status:MEDLINE


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[PMID]:28701511
[Au] Autor:Lawton SK; Xu F; Tran A; Wong E; Prakash A; Schumacher M; Hellman J; Wilhelmsen K
[Ad] Endereço:Biomedical Sciences Graduate Program, University of California, San Francisco, San Francisco, CA 94143.
[Ti] Título:-Arachidonoyl Dopamine Modulates Acute Systemic Inflammation via Nonhematopoietic TRPV1.
[So] Source:J Immunol;199(4):1465-1475, 2017 Aug 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:-Arachidonoyl dopamine (NADA) is an endogenous lipid that potently activates the transient receptor potential vanilloid 1 (TRPV1), which mediates pain and thermosensation. NADA is also an agonist of cannabinoid receptors 1 and 2. We have reported that NADA reduces the activation of cultured human endothelial cells by LPS and TNF-α. Thus far, in vivo studies using NADA have focused on its neurologic and behavioral roles. In this article, we show that NADA potently decreases in vivo systemic inflammatory responses and levels of the coagulation intermediary plasminogen activator inhibitor 1 in three mouse models of inflammation: LPS, bacterial lipopeptide, and polymicrobial intra-abdominal sepsis. We also found that the administration of NADA increases survival in endotoxemic mice. Additionally, NADA reduces blood levels of the neuropeptide calcitonin gene-related peptide but increases the neuropeptide substance P in LPS-treated mice. We demonstrate that the anti-inflammatory effects of NADA are mediated by TRPV1 expressed by nonhematopoietic cells and provide data suggesting that neuronal TRPV1 may mediate NADA's anti-inflammatory effects. These results indicate that NADA has novel TRPV1-dependent anti-inflammatory properties and suggest that the endovanilloid system might be targeted therapeutically in acute inflammation.
[Mh] Termos MeSH primário: Ácidos Araquidônicos/farmacologia
Dopamina/análogos & derivados
Inflamação/metabolismo
Canais de Cátion TRPV/metabolismo
[Mh] Termos MeSH secundário: Doença Aguda
Animais
Ácidos Araquidônicos/metabolismo
Peptídeo Relacionado com Gene de Calcitonina/sangue
Modelos Animais de Doenças
Dopamina/metabolismo
Dopamina/farmacologia
Inflamação/imunologia
Lipopeptídeos/imunologia
Lipopolissacarídeos/imunologia
Camundongos
Inibidor 1 de Ativador de Plasminogênio/metabolismo
Sepse/metabolismo
Substância P/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arachidonic Acids); 0 (Lipopeptides); 0 (Lipopolysaccharides); 0 (Plasminogen Activator Inhibitor 1); 0 (TRPV Cation Channels); 0 (TRPV1 protein, mouse); 0 (arachidonyl dopamine); 33507-63-0 (Substance P); 83652-28-2 (Calcitonin Gene-Related Peptide); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170714
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1602151



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