The role of protease-activated receptor type 2 in nociceptive signaling and pain

Title:

The role of protease-activated receptor type 2 in nociceptive signaling and pain

Creator:

Mrozkova, P., Palecek, J., and Spicarova, D.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:f9b54e3d-3ab2-4077-99b6-65d17210efe4
uuid:f9b54e3d-3ab2-4077-99b6-65d17210efe4
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, bolest, mícha, pain, spinal cord, protease-activated receptor (PAR2), signaling pathways, nociception, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

Protease-activated receptors (PARs) belong to the G-proteincoupled receptor family, that are expressed in many body tissues especially in different epithelial cells, mast cells and also in neurons and astrocytes. PARs play different physiological roles according to the location of their expression. Increased evidence supports the importance of PARs activation during nociceptive signaling and in the development of chronic pain states. This short review focuses on the role of PAR2 receptors in nociceptive transmission with the emphasis on the modulation at the spinal cord level. PAR2 are cleaved and subsequently activated by endogenous proteases such as tryptase and trypsin. In vivo, peripheral and intrathecal administration of PAR2 agonists induces thermal and mechanical hypersensitivity that is thought to be mediated by PAR2-induced release of pronociceptive neuropeptides and modulation of different receptors. PAR2 activation leads also to sensitization of transient receptor potential channels (TRP) that are crucial for nociceptive signaling and modulation. PAR2 receptors may play an important modulatory role in the development and maintenance of different pathological pain states and could represent a potential target for new analgesic treatments., P. Mrozkova, J. Palecek, D. Spicarova., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2016 Volume:65 | Number:3

Harvested from:

CDK

Metadata only:

false