| Institution: | 1. Department of Biotechnology, Asia University, Taichung, Taiwan
Department of Pediatrics, Ditmanson Medical Foundation Chia-Yi Christian Hospital, Chiayi, Taiwan;2. Institute of Oral Biology, National Yang-Ming University, Taipei, Taiwan;3. Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan;4. Department of Nursing, MeiHo University, Pingtung, Taiwan;5. Division of Cardiology, Department of Internal Medicine, Armed Force Taichung, General Hospital, Taichung, Taiwan;6. Department of Surgery, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan;7. Department of Biotechnology, Bharathiar University, Coimbatore, India;8. Department of Sports Sciences, University of Taipei, Taipei, Taiwan;9. Department of Biotechnology, Asia University, Taichung, Taiwan |
| 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. |
