Tid1-S attenuates LPS-induced cardiac hypertrophy and apoptosis through ER-a mediated modulation of p-PI3K/p-Akt signaling cascade

Chun Nun Chao, Jeng Fan Lo, Farheen B. Khan, Cecilia H. Day, Chao Hung Lai, Chia Hua Chen, Ray Jade Chen, Vijaya P. Viswanadha, Chia Hua Kuo, Chih Yang Huang

研究成果: 雜誌貢獻文章

摘要

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 pser473Akt. 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 ser473Akt 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.
原文英語
頁(從 - 到)16703-16710
頁數8
期刊Journal of Cellular Biochemistry
120
發行號10
DOIs
出版狀態已發佈 - 一月 1 2019

指紋

Cardiomegaly
Phosphatidylinositol 3-Kinases
Lipopolysaccharides
Modulation
Apoptosis
Proteins
Biological Phenomena
Cardiac Myocytes
Hypertrophy
Sepsis
Cells
Research

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

引用此文

Tid1-S attenuates LPS-induced cardiac hypertrophy and apoptosis through ER-a mediated modulation of p-PI3K/p-Akt signaling cascade. / Chao, Chun Nun; Lo, Jeng Fan; Khan, Farheen B.; Day, Cecilia H.; Lai, Chao Hung; Chen, Chia Hua; Chen, Ray Jade; Viswanadha, Vijaya P.; Kuo, Chia Hua; Huang, Chih Yang.

於: Journal of Cellular Biochemistry, 卷 120, 編號 10, 01.01.2019, p. 16703-16710.

研究成果: 雜誌貢獻文章

Chao, CN, Lo, JF, Khan, FB, Day, CH, Lai, CH, Chen, CH, Chen, RJ, Viswanadha, VP, Kuo, CH & Huang, CY 2019, 'Tid1-S attenuates LPS-induced cardiac hypertrophy and apoptosis through ER-a mediated modulation of p-PI3K/p-Akt signaling cascade', Journal of Cellular Biochemistry, 卷 120, 編號 10, 頁 16703-16710. https://doi.org/10.1002/jcb.28928
Chao, Chun Nun ; Lo, Jeng Fan ; Khan, Farheen B. ; Day, Cecilia H. ; Lai, Chao Hung ; Chen, Chia Hua ; Chen, Ray Jade ; Viswanadha, Vijaya P. ; Kuo, Chia Hua ; Huang, Chih Yang. / Tid1-S attenuates LPS-induced cardiac hypertrophy and apoptosis through ER-a mediated modulation of p-PI3K/p-Akt signaling cascade. 於: Journal of Cellular Biochemistry. 2019 ; 卷 120, 編號 10. 頁 16703-16710.
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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 pser473Akt. 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 ser473Akt 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.",
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AU - Khan, Farheen B.

AU - Day, Cecilia H.

AU - Lai, Chao Hung

AU - Chen, Chia Hua

AU - Chen, Ray Jade

AU - Viswanadha, Vijaya P.

AU - Kuo, Chia Hua

AU - Huang, Chih Yang

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AB - 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 pser473Akt. 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 ser473Akt 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.

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