scholarly journals Essential Role of Mast Cells in the Visceral Hyperalgesia Induced byT. spiralisInfection and Stress in Rats

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Chang-Qing Yang ◽  
Yan-Yu Wei ◽  
Chan-Juan Zhong ◽  
Li-Ping Duan
Keyword(s):  
Mast Cells ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Pcr Analysis ◽  
Signal Pathways ◽  
Transient Receptor Potential Vanilloid ◽  
Visceral Hyperalgesia ◽  
Cold Restraint Stress ◽  
Transient Receptor ◽  
Extracellular Regulated Kinase

Mast cells (MCs) deficient rats (Ws/Ws) were used to investigate the roles of MCs in visceral hyperalgesia. Ws/Ws and wild control (+/+) rats were exposed toT. spiralisor submitted to acute cold restraint stress (ACRS). Levels of proteinase-activated receptor 2 (PAR2) and nerve growth factor (NGF) were determined by immunoblots and RT-PCR analysis, and the putative signal pathways including phosphorylated extracellular-regulated kinase (pERK1/2) and transient receptor potential vanilloid receptor 1 (TRPV1) were further identified. Visceral hyperalgesia triggered by ACRS was observed only in+/+rats. The increased expression of PAR2 and NGF was observed only in+/+rats induced byT. spiralisand ACRS. The activation of pERK1/2 induced by ACRS occurred only in+/+rats. However, a significant increase of TRPV1 induced byT. spiralisand ACRS was observed only in+/+rats. The activation of PAR2 and NGF via both TRPV1 and pERK1/2 signal pathway is dependent on MCs in ACRS-induced visceral hyperalgesia rats.

scholarly journals Shaoyao-Gancao Decoction Relieves Visceral Hyperalgesia in TNBS-Induced Postinflammatory Irritable Bowel Syndrome via Inactivating Transient Receptor Potential Vanilloid Type 1 and Reducing Serotonin Synthesis

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Yun-Yun Shao ◽  
Yi-Ting Guo ◽  
Jian-ping Gao ◽  
Jun-Jin Liu ◽  
Zhuang-Peng Chang ◽  
...  
Keyword(s):  
Irritable Bowel Syndrome ◽  
Cell Count ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Low Grade ◽  
Visceral Hyperalgesia ◽  
Transient Receptor ◽  
Irritable Bowel ◽  
In Cells

Postinflammatory irritable bowel syndrome (PI-IBS) is a common functional gastrointestinal disorder, which is characterized by abdominal pain, low-grade inflammation, and visceral hypersensitivity. Shaoyao-Gancao decoction (SGD) has been used to improve the clinical symptoms of abdominal spasmodic pain accompanying acute gastroenteritis, but the underlying therapeutic mechanism has not been fully elucidated. In the present study, a rat model of PI-IBS was established via rectal administration of TNBS. Rats were scored daily for 28 days using disease activity index (DAI). Abdominal withdrawal reflex (AWR) was used to measure the pain threshold. After SGD (6.25, 12.5, and 25 g/kg/d) treatment for 14 days, rat colonic tissue was collected for histopathological grading, enterochromaffin (EC) cell count, and 5-HT content measurement. RT-qPCR and western blot analyses were employed to detect the gene and protein level of tryptophan hydroxylase (TPH), serotonin reuptake transporter (SERT), and transient receptor potential vanilloid 1 (TRPV1). To further validate the effect of SGD on TRPV1, another experiment was performed in cells. The results revealed that visceral hyperalgesia, reflected by increased DAI, AWR, pathological injury score, 5-HT content, and EC cell count in PI-IBS rats, was significantly ameliorated by SGD. In cells, SGD markedly inhibited the expression and function of TRPV1. Moreover, the expression levels of TPH were also repressed by SGD. The findings of the present study indicated that the therapeutic effect of SGD on visceral hyperalgesia may be closely associated with the regulatory role of TRPV1 and 5-HT signaling pathways.

scholarly journals A TRPV2–PKA Signaling Module for Transduction of Physical Stimuli in Mast Cells

2004 ◽  
Vol 200 (2) ◽  
pp. 137-147 ◽  
Author(s):  
Alexander J. Stokes ◽  
Lori M.N. Shimoda ◽  
Murielle Koblan-Huberson ◽  
Chaker N. Adra ◽  
Helen Turner
Keyword(s):  
Mast Cells ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Functional Coupling ◽  
Transient Receptor Potential Vanilloid ◽  
Functional Responses ◽  
Signaling Mechanism ◽  
Cutaneous Mast Cell ◽  
Transient Receptor

Cutaneous mast cell responses to physical (thermal, mechanical, or osmotic) stimuli underlie the pathology of physical urticarias. In vitro experiments suggest that mast cells respond directly to these stimuli, implying that a signaling mechanism couples functional responses to physical inputs in mast cells. We asked whether transient receptor potential (vanilloid) (TRPV) cation channels were present and functionally coupled to signaling pathways in mast cells, since expression of this channel subfamily confers sensitivity to thermal, osmotic, and pressure inputs. Transcripts for a range of TRPVs were detected in mast cells, and we report the expression, surface localization, and oligomerization of TRPV2 protein subunits in these cells. We describe the functional coupling of TRPV2 protein to calcium fluxes and proinflammatory degranulation events in mast cells. In addition, we describe a novel protein kinase A (PKA)–dependent signaling module, containing PKA and a putative A kinase adapter protein, Acyl CoA binding domain protein (ACBD)3, that interacts with TRPV2 in mast cells. We propose that regulated phosphorylation by PKA may be a common pathway for TRPV modulation.

Moxibustion Relieves Visceral Hyperalgesia via Inhibition of Transient Receptor Potential Vanilloid 1 (Trpv1) and Heat Shock Protein (Hsp) 70 Expression in Rat Bone Marrow Cells

2016 ◽  
Vol 34 (2) ◽  
pp. 114-119 ◽  
Author(s):  
Weiying Zou ◽  
Hua Lin ◽  
Wenwen Liu ◽  
Bei Yang ◽  
Lei Wu ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Transient Receptor Potential ◽  
Bone Marrow Cells ◽  
Acupuncture Point ◽  
Receptor Potential ◽  
Hsp70 Expression ◽  
Transient Receptor Potential Vanilloid ◽  
Visceral Hyperalgesia ◽  
Transient Receptor ◽  
Marrow Cells

Objective To investigate the effects of moxibustion on visceral hyperalgesia (VH) and bone marrow cell transient receptor potential vanilloid type 1 (TRPV1) and heat shock protein (HSP) 70 expression in a rat model of VH. Methods Mechanical colorectal distension was performed to induce VH in neonatal Sprague-Dawley rats. Eight-week-old VH rats were treated with moxibustion at acupuncture point BL25 or an ipsilateral non-acupuncture point. Abdominal withdrawal reflex (AWR) scoring and pain threshold pressure assessment were performed before and after moxibustion treatment for 7 consecutive days. The expression of TRPV1 and HSP70 in bone marrow cells was quantified by real-time quantitative PCR. Results The expression of TRPV1 and HSP70 in bone marrow cells was increased in rats with VH. Moxibustion at BL25 significantly decreased AWR scores and increased pain threshold pressure in rats with VH. Furthermore, moxibustion at BL25 significantly inhibited the VH-induced increase in the expression of TRPV1 and HSP70 in bone marrow cells. Conclusions The up-regulation of TRPV1 and HSP70 expression in bone marrow cells may be involved in visceral pain development and the analgesic effect of moxibustion on VH may be mediated through down-regulation of TRPV1 and HSP70 expression in bone marrow cells.

scholarly journals Manual Acupuncture at ST37 Modulates TRPV1 in Rats with Acute Visceral Hyperalgesia via Phosphatidylinositol 3-Kinase/Akt Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Caiyi Chen ◽  
Zhi Yu ◽  
Dong Lin ◽  
Xuan Wang ◽  
Xuejun Zhang ◽  
...  
Keyword(s):  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Vital Role ◽  
Akt Pathway ◽  
Transient Receptor Potential Vanilloid ◽  
Manual Acupuncture ◽  
Phosphatidylinositol 3 Kinase ◽  
Visceral Hyperalgesia ◽  
Transient Receptor ◽  
Phosphatidylinositol 3

Acupuncture can significantly ameliorate inflammatory pain in acute visceral hyperalgesia. Hyperalgesia is attenuated by inflammatory mediators that activate transient receptor potential vanilloid 1 (TRPV1), and TRPV1 is regulated by nerve growth factor (NGF)-induced phosphatidylinositol 3-kinase (PI3K)/Akt pathway. However, it is unknown whether NGF-induced PI3K/Akt pathway is associated with manual acupuncture (MA). In this study, the effect and mechanism of MA at Shangjuxu (ST37) and Quchi (LI11) were examined using an acetic acid-induced rat model with visceral hyperalgesia. We demonstrated that MA at ST37 significantly decreased abdominal withdrawal reflex (AWR) scores, proinflammatory cytokine expression (TNF-α, IL-1β, and IL-6), and TRPV1 protein and mRNA expression in rats with acute visceral hyperalgesia compared with the untreated controls, while MA at LI11 showed no effect. The effects of MA at ST37 were reversed after treatment with the PI3K agonist IGF-1 30 min before MA. In rats with visceral hyperalgesia, the upregulation of NGF, tropomyosin-receptor-kinase A (TrkA), PI3K, and phosphorylation-Akt (p-Akt) was decreased by MA at ST37, indicating that TRPV1 regulation via the NGF-induced PI3K/Akt pathway plays a vital role in the effects of MA-mediated amelioration of acute visceral hyperalgesia.

scholarly journals L-carnitine suppresses transient receptor potential vanilloid type 1 activity and myofibroblast transdifferentiation in human corneal keratocytes

2021 ◽  
Author(s):  
Elizabeth Turan ◽  
Monika Valtink ◽  
Peter S. Reinach ◽  
Annett Skupin ◽  
Huan Luo ◽  
...  
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Transient Receptor Potential ◽  
Smooth Muscle Actin ◽  
Receptor Potential ◽  
Pcr Analysis ◽  
Transient Receptor Potential Vanilloid ◽  
Alpha Smooth Muscle Actin ◽  
Transient Receptor ◽  
Corneal Keratocytes

AbstractCorneal stromal wound healing is a well-balanced process promoted by overlapping phases including keratocyte proliferation, inflammatory-related events, and tissue remodeling. L-carnitine as a natural antioxidant has shown potential to reduce stromal fibrosis, yet the underlying pathway is still unknown. Since transient receptor potential vanilloid 1 (TRPV1) is a potential drug target for improving the outcome of inflammatory/fibrogenic wound healing, we investigated if L-carnitine can mediate inhibition of the fibrotic response through suppression of TRPV1 activation in human corneal keratocytes (HCK). We determined TRPV1-induced intracellular calcium transients using fluorescence calcium imaging, channel currents by planar patch-clamping, and cell migration by scratch assay for wound healing. The potential L-carnitine effect on TRPV1-induced myofibroblast transdifferentiation was evaluated by immunocytochemical detection of alpha smooth muscle actin. RT-PCR analysis confirmed TRPV1 mRNA expression in HCK. L-carnitine (1 mmol/l) inhibited either capsaicin (CAP) (10 µmol/l), hypertonic stress (450 mOsmol/l), or thermal increase (>43 °C) induced Ca2+ transients and corresponding increases in TRPV1-induced inward and outward whole-cell currents. This was accompanied by suppression of injury-induced increases in myofibroblast transdifferentiation and cell migration. In conclusion, L-carnitine contributes to inhibit stromal scarring through suppressing an injury-induced intrinsic TRPV1 activity that is linked with induction of myofibroblast transdifferentiation in HCK cells.

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