Transient receptor potential ankyrin 1 activation enhances hapten sensitization in a T-helper type 2-driven fluorescein isothiocyanate-induced contact hypersensitivity mouse model

2012 ◽  
Vol 264 (3) ◽  
pp. 370-376 ◽  
Author(s):  
Takahiro Shiba ◽  
Takuma Tamai ◽  
Yurina Sahara ◽  
Kohta Kurohane ◽  
Tatsuo Watanabe ◽  
...  
Keyword(s):  
Mouse Model ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Fluorescein Isothiocyanate ◽  
Contact Hypersensitivity ◽  
T Helper ◽  
Transient Receptor ◽  
Helper Type

scholarly journals Transient receptor potential melastatin 2 governs stress-induced depressive-like behaviors

2019 ◽  
Vol 116 (5) ◽  
pp. 1770-1775 ◽  
Author(s):  
Seung Yeon Ko ◽  
Sung Eun Wang ◽  
Han Kyu Lee ◽  
Sungsin Jo ◽  
Jinil Han ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Synaptic Function ◽  
Tissue Samples ◽  
Transient Receptor Potential Melastatin ◽  
Transient Receptor ◽  
The Brain ◽  
Synapsin 1

Major depressive disorder (MDD) is a devastating disease that arises in a background of environmental risk factors, such as chronic stress, that produce reactive oxygen species (ROS) in the brain. The chronic stress-induced ROS production involves Ca2+ signals; however, the mechanism is poorly understood. Transient receptor potential melastatin type 2 (TRPM2) is a Ca2+-permeable cation channel that is highly expressed in the brain. Here we show that in animal models of chronic unpredictable stress (CUS), deletion of TRPM2 (Trpm2−/−) produces antidepressant-like behaviors in mice. This phenotype correlates with reduced ROS, ROS-induced calpain activation, and enhanced phosphorylation of two Cdk5 targets including synapsin 1 and histone deacetylase 5 that are linked to synaptic function and gene expression, respectively. Moreover, TRPM2 mRNA expression is increased in hippocampal tissue samples from patients with MDD. Our findings suggest that TRPM2 is a key agent in stress-induced depression and a possible target for treating depression.

Gene variation of the transient receptor potential cation channel, subfamily M, member 2 (TRPM2) and type 2 diabetes mellitus: A case–control study

2010 ◽  
Vol 411 (19-20) ◽  
pp. 1437-1440 ◽  
Author(s):  
José R. Romero ◽  
Soren Germer ◽  
Amy J. Castonguay ◽  
Nathaniel S. Barton ◽  
Mitchell Martin ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Transient Receptor Potential ◽  
Case Control Study ◽  
Receptor Potential ◽  
Case Control ◽  
Gene Variation ◽  
Transient Receptor ◽  
Control Study

scholarly journals Periorbital nociception in a progressive multiple sclerosis mouse model is dependent on TRPA1 channel activation

2021 ◽  
Author(s):  
Diéssica Padilha Dalenogare ◽  
Diulle Spat Peres ◽  
Maria Fernanda Pessano Fialho ◽  
Gabriela Trevisan dos Santos
Keyword(s):  
Multiple Sclerosis ◽  
Mouse Model ◽  
Mechanical Allodynia ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Progressive Multiple Sclerosis ◽  
Autoimmune Encephalomyelitis ◽  
Transient Receptor ◽  
Multiple Sclerosis Patients ◽  
Santa Maria

Background: Headache is one of the main painful symptoms described by multiple sclerosis patients. Previously, it was described that neuropathic pain-like behaviors were dependent on transient receptor potential ankyrin 1 (TRPA1) activation in a progressive multiple sclerosis model induced by experimental autoimmune encephalomyelitis (PMS- EAE) in mice. Objective: Here, we aimed to investigate if periorbital mechanical allodynia induced by PMS-EAE was also related to TRPA1 activation. Design and setting: Federal University of Santa Maria, Santa Maria, RS, Brazil. Methods: To induce a PMS-EAE we used female C57BL/6 wild-type and TRPA1- deficient (Trpa1-/-) mice. By the von Frey test, periorbital mechanical allodynia development was observed, and the nociception peak occurred 14 days after induction. At nociception peak day, the mice were treated with sumatriptan, TRPA1 antagonists (HC-030031, A-967079, metamizole, and propyphenazone. Results: The development of mechanical allodynia was showed as well as the antinociceptive effects for all treatments in induced mice. A significant reduction of TRPA1 expression was detected. Conclusion: Thus, these results suggest that headache-like symptoms induced by the PMS-EAE mouse model might occurring by TRPA1 activation.

Non-electrophilic TRPA1 agonists, menthol, carvacrol and clotrimazole, open epithelial tight junctions via TRPA1 activation

2020 ◽  
Vol 168 (4) ◽  
pp. 407-415
Author(s):  
Minagi Mukaiyama ◽  
Takeo Usui ◽  
Yoko Nagumo
Keyword(s):  
Tight Junctions ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Fluorescein Isothiocyanate ◽  
Epithelial Permeability ◽  
Food Ingredients ◽  
Transient Receptor Potential A1 ◽  
Epithelial Barriers ◽  
Transient Receptor ◽  
Permeability Enhancers

Abstract Activation of the transient receptor potential A1 channel (TRPA1) by electrophilic agonists was reported to induce the opening of tight junctions (TJs). Because compounds that increase TJ permeability can be paracellular permeability enhancers, we investigated the effect of non-electrophilic TRPA1 activators, including food ingredients (menthol and carvacrol) and medication (clotrimazole), on epithelial permeability. We show that all three compounds induced increase of the permeability of fluorescein isothiocyanate-conjugated dextran (4 kDa) and decrease of transepithelial electrical resistance, accompanied by Ca2+ influx and cofilin activation in epithelial MDCK II monolayers. These phenotypes were attenuated by pretreatment of a TRPA1 antagonist, suggesting TRPA1-mediated opening of TJs. These results suggest that non-electrophilic TRPA1 activators with established safety can be utilized to regulate epithelial barriers.

Sign in / Sign up

Export Citation Format

Share Document