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Tid1‐S attenuates LPS‐induced cardiac hypertrophy and apoptosis through ER‐a mediated modulation of p‐PI3K/p‐Akt signaling cascade
Author(s) -
Chao ChunNun,
Lo JengFan,
Khan Farheen B.,
Day Cecilia H.,
Lai ChaoHung,
Chen ChiaHua,
Chen RayJade,
Viswanadha Vijaya P.,
Kuo ChiaHua,
Huang ChihYang
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28928
Subject(s) - protein kinase b , pi3k/akt/mtor pathway , apoptosis , microbiology and biotechnology , signal transduction , muscle hypertrophy , cancer research , medicine , chemistry , endocrinology , biology , biochemistry
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.