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.
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