Cobalt Chloride-Induced Tissue Regeneration and Wound Healing Depend on HIF-1α and VEGF-A-Mediated Neovascularization.

Abstract

The study investigates the role of cobalt chloride (CoCl₂), a hypoxia-inducing agent, in promoting tissue regeneration using zebrafish as a model system. Caudal fins of adult zebrafish were amputated and transdermally exposed to 1% CoCl₂. The extent of fin regeneration and the neovascularization process at the growth front were analyzed. CoCl₂ exposure significantly enhanced regeneration compared with controls, with increased fin length and more prominent blood vessel sprouting and anastomosis. Molecular and proteomics analyses revealed an upregulation of angiogenic and pro-angiogenic factors, particularly Vascular Endothelial Growth Factor (VEGF). To verify the role of VEGF in CoCl₂-mediated tissue regeneration, the amputated fins were exposed to inhibitors such as genistein and SU5416. These results suggest that CoCl₂ promotes tissue regrowth and wound healing by stimulating angiogenesis. The findings highlight the therapeutic potential of CoCl₂ in enhancing regeneration and wound repair through the HIF-1α/VEGF signaling pathway, with potential implications for treating ischemic wounds.