Transient receptor potential (TRP) channels function in diverse processes such as acting as second messenger systems, regulating of ionic concentrations, and aiding in thermoception. TRPM2 channels, members of the melastatin subfamily, mediate calcium influx in response to oxidative stress but during pathological states facilitate hyperexcitability and cellular necrosis via calcium excitotoxicity. We hypothesized that TRPM2 channel expression is upregulated in pulpal tissue of symptomatic teeth with signs of irreversible pulpitis. TRPM2 channel expression was significantly increased in pulp from clinically diagnosed symptomatic teeth compared with pulp from asymptomatic teeth. Additionally, increased TRPM2 expression in symptomatic pulp was the result of increased immunoreactivity in fibroblasts, whereas neural expression of TRPM2 was absent. We provide a possible mechanism explaining the association between TRPM2 channel expression with pain and necrosis. We suggest that TRPM2 channel antagonists could be administered in attempts to inhibit the progression of or even reverse pulpal degradation.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.joen.2006.11.020 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Immunohistochemical investigation of transient receptor potential melastatin-2 and spexin immunoreactivity in atopic dermatitis and mycosis fungoides.
Arch Dermatol Res
January 2025
Department of Dermatology, Firat University Hospital, Elazig, TR23119, Turkey.
Background: Atopic dermatitis (AD) is a chronic, pruritic, and inflammatory dermatosis seen in individuals with an atopic predisposition. This study aimed to examine the immunoreactivity of spexin and TRPM2 in skin samples from patients with AD and MF lesions using immunohistochemical methods.
Materials And Methods: The study utilized a total of 60 skin samples, comprising 20 from AD patients, 20 from MF patients, and 20 from control subjects.
Downregulation and inhibition of TRPM2 calcium channel prevent oxidative stress-induced endothelial dysfunction in the EA.hy926 endothelial cells model - Preliminary studies.
Adv Med Sci
January 2025
Department of Histology and Embryology, Faculty of Medicine, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Toruń, Toruń, Poland; Faculty of Medicine, Collegium Medicum, Mazovian Academy in Płock, Płock, Poland.
Purpose: Proper functioning of the endothelial barrier is crucial for cardiovascular system homeostasis. Oxidative stress can lead to endothelial dysfunction (ED), damaging lipids, proteins, and DNA. Reactive oxygen species also increase cytoplasmic Ca levels, activating transient receptor potential melastatin 2 (TRPM2), a membrane non-selective calcium channel.
View Article and Find Full Text PDFSlick potassium channels limit TRPM3-mediated activation of sensory neurons.
Front Pharmacol
December 2024
Institute of Pharmacology and Clinical Pharmacy, Goethe University Frankfurt, Frankfurt, Germany.
Article Synopsis
- Specialized heat-sensitive neurons in the skin relay heat sensations, with the sodium-activated potassium channel Slick playing a significant role in controlling noxious heat responses.
- Researchers created mice lacking Slick in specific sensory neurons (SNS-Slick mice) and found these mice had quicker responses to painful heat tests compared to normal mice.
- Further experiments revealed that Slick works alongside the heat sensor TRPM3, suggesting that Slick helps to inhibit pain responses by modulating TRPM3 activity in sensory neurons.
Mechanism of action of curcumin targeting TRPM2/NLRP3 signaling axis to mediate cell death in the treatment of knee osteoarthritis.
Hum Exp Toxicol
December 2024
Department of Orthopedics, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, China.
Objects: This study intends to explore the possible mechanisms of curcumin's action after knee osteoarthritis.
Methods: Chondrocytes alone were used to mimic the cellular inflammatory response with interleukin IL-1β. Overexpressing TRPM2 chondrocytes were constructed using cell transfection technique for mechanism verification.
TRPM2 deficiency ameliorated H9N2 influenza virus-induced acute lung injury in mice.
Microb Pathog
November 2024
Key Laboratory of Preventive Veterinary Medicine, Department of Veterinary Medicine, Animal Science College, Hebei North University, Zhangjiakou, 075000, Hebei, PR China. Electronic address:
Oxidative stress is involved in lung damage induced by the influenza virus. The transient receptor potential melastatin-2 (TRPM2) cation channel, a Ca permeable non-selective cation channel, is implicated in the mediation of multiple tissue injuries induced by oxidative stress. The role of TRPM2 in several diseases has been widely studied, but there have been few studies on the involvement of TRPM2 in lung injury induced by the H9N2 influenza virus.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!