实验证据表明，F/F ATP 酶的参与以及随后的 P2Y 受体激活，在胸腺素原 α 诱导的视网膜缺血损伤保护中起作用。

Experimental evidence for the involvement of F/F ATPase and subsequent P2Y receptor activation in prothymosin alpha-induced protection of retinal ischemic damage.

机构信息

Department of Pharmacology and Therapeutic Innovation, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki 852-8521, Japan; San Diego Biomedical Research Institute, 10865 Road to the Cure #100, San Diego, CA 92121, USA.

Department of Pharmacology and Therapeutic Innovation, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki 852-8521, Japan; Department of Medical Pharmacology, Nagasaki University of Graduate School of Biomedical Sciences, Nagasaki 852-8523, Japan.

出版信息

J Pharmacol Sci. 2020 Jun;143(2):127-131. doi: 10.1016/j.jphs.2020.01.008. Epub 2020 Feb 27.

DOI:10.1016/j.jphs.2020.01.008

PMID:32156464

Abstract

The inhibition of retinal ischemia-induced damage by post-ischemic prothymosin alpha (ProTα) was not affected in toll-like receptor 4 knockout (TLR4) mice but blocked by the pretreatment with antibody against F/F ATPase α- or β-subunit, novel candidate for ProTα-receptor. In addition to the previous observation of ProTα-induced ATP release from cells, the present study showed a ProTα-induced enhancement of ATP hydrolysis activity of recombinant ATP5A1/5B complex. As the protection of retinal function by post-ischemic ProTα was abolished by anti-P2Y antibody, the activation of F/F ATPase and subsequent P2Y receptor system may play roles in beneficial actions by post-ischemic ProTα.

摘要

缺血后胸腺肽原 α（ProTα）对视网膜缺血损伤的抑制作用在 Toll 样受体 4 敲除（TLR4）小鼠中不受影响，但用针对 F/F ATP 酶 α-或 β-亚基的抗体预处理可阻断，F/F ATP 酶 α-或 β-亚基是 ProTα 受体的新候选物。除了先前观察到 ProTα 诱导细胞释放 ATP 之外，本研究还显示 ProTα 诱导重组 ATP5A1/5B 复合物的 ATP 水解活性增强。由于缺血后 ProTα 对视网膜功能的保护作用被抗 P2Y 抗体所消除，因此 F/F ATP 酶的激活和随后的 P2Y 受体系统可能在缺血后 ProTα 的有益作用中发挥作用。