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Jnk1 regulate jun protein turnover9/10/2023 ![]() ![]() Myocardial Infarction (MI) is a leading cause of morbidity and mortality in industrialized countries ( Guo et al., 2016). Overall, the results of our study demonstrate that the wnt2bb-mediated jnk1/c-jun/creb1 non-canonical Wnt pathway regulates cardiomyocyte proliferation. In addition, wnt2bb/jnk1/c-jun/creb1 signaling was increased in Tg(hsp70l:dkk1) transgenic fish, whereas it was inhibited in Tg(hsp70l:wnt8) transgenic fish, indicating that canonical Wnt and non-canonical Wnt antagonize each other to regulate heart regeneration. The overexpression of creb1 sufficiently rescued the dn-wnt2bb-induced phenotype of reduced nkx2.5 expression and attenuated heart regeneration. The expression of jnk1, creb1, and c-jun were inhibited in wnt2bb dominant negative (dn) mutant hearts and elevated in wnt2bb-overexpresssing hearts following ventricular amputation. In this study, we have demonstrated that inhibition of injury-induced myocardial wnt2bb and jnk1/creb1/c-jun signaling impedes heart repair following apex resection. However, the mechanism by which Wnt signaling regulates downstream gene expression following heart injury remains unknown. Previous studies have demonstrated that inhibition of canonical Wnt signaling promotes zebrafish heart regeneration and that treatment of injured heart tissue with the Wnt activator 6-bromo-indirubin-3-oxime (BIO) can impede cardiomyocyte proliferation. 3Guangdong Engineering & Technology Research Center for Disease-Model Animals, Laboratary Animal Center, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.2Heart Center, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou, China.1Guangzhou Women and Children’s Medical Centre, Institute of Pediatrics, Guangzhou Medical University, Guangzhou, China.Xiangwen Peng 1† Shunyang Fan 2† Jing Tan 3 Zhi Zeng 1 Meiling Su 1 Yuan Zhang 1 Ming Yang 3 Luoxing Xia 1 Xuejiao Fan 1 Weibin Cai 3* Wai Ho Tang 1* ![]()
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