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

0462321 - FGÚ 2017 RIV CZ eng J - Článek v odborném periodiku
Mrózková, Petra - Paleček, Jiří - Špicarová, Diana
The role of protease-activated receptor type 2 in nociceptive signaling and pain.
Physiological Research. Roč. 65, č. 3 (2016), s. 357-367. ISSN 0862-8408. E-ISSN 1802-9973
Grant CEP: GA MŠMT(CZ) LH12058; GA ČR(CZ) GBP304/12/G069; GA ČR(CZ) GA15-11138S; GA MŠMT(CZ) LH15279; GA MŠMT(CZ) ED1.1.00/02.0109
Institucionální podpora: RVO:67985823
Klíčová slova: protease-activated receptor (PAR2) * signaling pathways * nociception * pain * spinal cord
Kód oboru RIV: FH - Neurologie, neurochirurgie, neurovědy
Impakt faktor: 1.461, rok: 2016

Protease-activated receptors (PARs) belong to the G-protein-coupled 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.
Trvalý link: http://hdl.handle.net/11104/0261793