Pannexin 1 is a participant of purinergic signaling in murine basilar arteryстатьяТезисы
Статья опубликована в высокорейтинговом журнале
Информация о цитировании статьи получена из
Web of Science,
Scopus
Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 20 декабря 2019 г.
Аннотация:Pannexin 1 (Panx1) is a new player in vascular tone regulation, but the pattern of its expression|/functioning differs among the vascular beds. Surprisingly, vasomotor role of Panx1 has not been studied in cerebral arteries, although Panx1 in abundant in the central nervous system. Therefore, our study was aimed at the role of Panx1 in purinergic control of murine basilar artery (BA) tone. Experiments were performed on BA from 2-3-month-old male Panx1 knockout (KO) and C57BL/6 (WT) mice. The arterial segments were mounted in wire myograph (DMT). ATP- and acetylcholine (ACh)-induced relaxation was studied in U46619- precontracted arteries. The contribution of ATP/ADP was dissected using apyrase (ATPase/ADPase) and 8-SPT (adenosine receptor blocker). The content of CD39 mRNA was studied using qPCR (Corbett Research). Contractile response to ATP (10 microM) was higher in KO compared to WT (27% and 39% from the maximum contractile force, respectively). In precontracted BA, ATP (30 microM) induced biphasic effect: transient contraction was followed by relaxation, which also was increased in KO compared to WT (38% and 19% from the precontraction level, respectively). Apyrase in combination with 8-SPT decreased the response to ACh in WT but not in KO, while 8-SPT alone had not effect in either group. The level of CD39 mRNA in cerebral arteries was lower in KO compared to WT. Our data suggest, that Panx1 has important role in purinergic control of BA tone through ATP/ADP secretion. The ablation of Panx1 augments vasomotor responses to ATP, probably, as a result of the decline of CD39, a principal ectonucleotidase in murine arteries. Importantly, Panx1 participates in endothelium-dependent relaxiation of BA to vasoactive ligands.