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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. However, the mechanism by which Wnt signaling regulates downstream gene expression following heart injury remains unknown. 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. 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. The overexpression of  creb1  sufficiently rescued the  dn-wnt2bb -induced phenotype of reduced  nkx2.5  expression and attenuated heart regeneration. 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. Overall, the results of our study demonstrate that the wnt2bb-mediated  jnk1/c-jun/creb1  non-canonical Wnt pathway regulates cardiomyocyte proliferation.

Wnt2bb Induces Cardiomyocyte Proliferation in Zebrafish Hearts via the jnk1/c-jun/creb1 Pathway