A knock-in mutation at cysteine 144 of TRIM72 is cardioprotective and reduces myocardial TRIM72 release

TRIM72 is a membrane repair protein that protects against ischemia reperfusion (I/R) injury. We previously identified Cys144 (C144) on TRIM72 as a site of S-nitrosylation. To study the importance of C144, we generated a knock-in mouse with C144 mutated to a serine (TRIM72 C144S). We subjected ex vivo perfused mouse hearts to 20  min of ischemia followed by 90 min of reperfusion and observed less injury in TRIM72 C144S compared to WT hearts. Infarct size was smaller (54 vs 27% infarct size) and cardiac functional recovery (37 vs 62% RPP) was higher for the TRIM72 C144S mouse hearts.

Source: Journal of Molecular and Cellular Cardiology - September 15, 2019 Category: Cytology Authors: Natasha Fillmore, Kevin M. Casin, Prithvi Sinha, Junhui Sun, Hanley Ma, Jennifer Boylston, Audrey Noguchi, Chengyu Liu, Nadan Wang, Guangshuo Zhou, Mark J. Kohr, Elizabeth Murphy Source Type: research