文章基本信息

标题：TRPM7 in CHBP-induced renoprotection upon ischemia reperfusion-related injury
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作者：Aifen Liu ; Jing Wu ; Cheng Yang 等
期刊名称：Scientific Reports
电子版ISSN：2045-2322
出版年度：2018
卷号：8
期号：1
页码：5510
DOI：10.1038/s41598-018-22852-2
语种：English
出版社：Springer Nature
摘要：Transient receptor potential melastatin 7 (TRPM7) is a membrane ion channel and kinase. TRPM7 was abundantly expressed in the kidney, and up-regulated by ischemia reperfusion (IR) injury. Our previous studies showed that cyclic helix B peptide (CHBP) improved renal IR-related injury, but its underlying mechanism is not well defined. IR-related injury was established in renal tubular epithelial cells (TCMK-1 and HK-2) via 12 to 24-h hypoxia (H) followed by 2-24 h reoxygenation (R), and in mouse kidneys subjected to 30-min ischemia and 12-h to 7-day reperfusion. TRPM7-like current in TCMK-1 cells, TRPM7 mRNA and protein in the in vitro and in vivo models were increased, but reversed by CHBP. TRPM7 was also positively associated with LDH, HMGB1, caspase-3, Bax/Bcl-2, inflammation, apoptosis, tubulointerstitial damage and renal function respectively. Furthermore, silencing TRPM7 improved injury parameters, renal histology and function in the both models. Specific TRPM7 agonist, bradykinin, exaggerated HR induced injury in TCMK-1 cells, and partially blocked the renoprotection of CHBP as well. In conclusion, TRPM7 is involved not only in IR-related injury, but also CHBP-induced renoprotection, which are through its ion channel and subsequent affects inflammation and apoptosis. Therefore, TRPM7 could be a potential biomarker for IR-induced acute kidney injury.