In:
Journal of Cellular Biochemistry, Wiley, Vol. 120, No. 10 ( 2019-10), p. 16703-16710
Abstract:
Myocardial dysfunction is clinically relevant? repercussion that follows sepsis. Tid 1 protein has been implicated in many biological process. However, the role of Tid 1 in lipopolysaccharide (LPS)‐induced cardiomyocyte hypertrophy and apoptosis remains elusive. In the current research endeavor, we have elucidated the role of Tid1‐S on LPS‐induced cardiac hypertrophy and apoptosis. Interestingly, we found that overexpression of Tid1‐S suppressed TLR‐4, NFATc3, and BNP protein expression which eventually led to inhibition of LPS‐induced cardiac hypertrophy. Moreover, Tid1‐S overexpression attenuated cellular apoptosis and activated survival proteins p‐PI3K and p ser473 Akt. Besides this, Tid1‐S overexpression enhanced ER‐a protein expression. Collectively, our data suggest that Tid1‐S plausibly enhance ER‐a protein and further activate p‐PI3K and p ser473 Akt survival protein expression; which thereby led to attenuation of LPS‐induced apoptosis in cardiomyoblast cells. Interestingly, our data suggest that Tid1‐S is involved in attenuation of cardiomyoblast cells damages induced by LPS.
Type of Medium:
Online Resource
ISSN:
0730-2312
,
1097-4644
Language:
English
Publisher:
Wiley
Publication Date:
2019
detail.hit.zdb_id:
1479976-5
SSG:
12
