Abstract
Endoplasmic reticulum (ER) stress and subsequent apoptosis play a vital role in myocardial ischemia reperfusion (IR) injury. Fatty acid binding protein 4 (FABP4) may induce ER stress. The aim of this study was to investigate the mechanism and effect of FABP4 on IR injury in vitro. Rat H9c2 cells were exposed to hypoxia reoxygenation (HR) to create an IR model in vitro. FABP4 was overexpressed in HR-injured H9c2 cells. Transfection with FABP4 siRNA increased cell viability and decreased LDH upon HR stimulation. FABP4 cessation also suppressed apoptotic cells and caspase-3 activity after HR. Downregulation of FABP4 significantly inhibited ER stress by decreasing the protein expression of p-PERK, GRP78, and ATF6. FABP4 silencing also restrained the ER stress-mediated apoptotic pathway, as indicated by decreased pro-apoptotic proteins p-JNK, CHOP, Bax, and caspase-12, as well as upregulation of Bcl-2 during HR. Furthermore, FABP4 silencing activated the PI3K/Akt pathway. Blocking this pathway by the specific PI3K inhibitor-LY294002 restored HR-induced ER stress and subsequently reversed the protective effect of FABP4 silencing on HR injury. Taken together, our findings revealed that FABP4 silencing exerts protective effects against HR injury in H9c2 cells through inhibiting ER stress-induced cell apoptosis via activation of the PI3K/Akt pathway.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
