Abstract
We have already reported that IL‐10 prevents TNF‐α induced increase in oxidative stress and apoptosis in cardiomyocytes. Present study investigated the role of Akt and Jak/Stat pathway in IL‐10 mediated survival of cardiomyocytes. Isolated cardiomyocytes from adult Sprague Dawley rats were exposed to TNF‐α (10ng/ml), IL‐10 (10ng/ml) and TNF‐α+IL‐10 (ratio 1) for 4h. Exposure to TNF‐α resulted in decrease in cell viability and an increase in cardiomyocyte apoptosis. IL‐10 by itself had no effect, but it prevented TNF‐α induced cardiomyocyte apoptosis and enhanced the cell survival. Furthermore, IL‐10 treatment increased Akt levels within cardiomyocytes and this change was associated with an increase in Jak1 and Stat3 phosphorylation. Pre‐exposure of cells to Akt/or Stat3 inhibitor prevented IL‐10 modulation of TNF‐α induced cardiomyocyte apoptosis. Furthermore, in the presence of Akt inhibitor IL‐10 treatment was unable to induce Stat3 phosphorylation. It is concluded that Akt regulates IL‐10 mediated survival of cardiomyocytes by upregulating Stat3 phosphorylation (Supported by CIHR‐IMPACT, Canada).
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.
