Tail regeneration is a distinguishing feature of lizards; however, the mechanisms underlying tail regeneration remain elusive. Prostaglandin E2 (PGE2) is an arachidonic acid metabolite that has been extensively investigated in the inflammatory response under both physiological and pathological conditions. PGE2 also act as a regulator of hematopoietic stem cell homeostasis by interacting with Wnt signaling molecules. The present study aims to identify the effects of PGE2 on tail regeneration and the molecular mechanisms behind it. We initially found that PGE2 levels increased during the early stages of tail regeneration, accompanied by the up-regulated expression of cyclooxygenase 1 and cyclooxygenase 2. Next, we demonstrated that reduced PGE2 production leads to the retardation of tail regeneration. Subsequent experiments demonstrated that this effect is likely mediated by Wnt signaling, which proposing that the activation of the Wnt pathway is essential for the initiation of regeneration. The results showed that inhibition of PGE2 production could suppress Wnt activation and inhibit the proliferation of both epithelial and blastema cells. Furthermore, our findings indicated that forced activation of Wnt signaling could rescue the inhibitory effect of Cox antagonist on regeneration, suggesting a positive role of PGE2 on tail regeneration via a non-inflammatory mechanism.

中文翻译：

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PGE2通过激活日本壁虎中的Wnt信号来促进尾巴再生。

尾巴再生是蜥蜴的一个显着特征。然而，尾巴再生的机制仍然难以捉摸。前列腺素E2（PGE2）是一种花生四烯酸代谢产物，已在生理和病理条件下对炎症反应进行了广泛研究。PGE2还通过与Wnt信号分子相互作用，充当造血干细胞稳态的调节剂。本研究旨在确定PGE2对尾巴再生的影响及其背后的分子机制。我们最初发现，在尾巴再生的早期阶段，PGE2水平升高，同时伴随着环氧合酶1和环氧合酶2的表达上调。接下来，我们证明了降低的PGE2产生会导致尾巴再生的延迟。随后的实验表明，这种作用可能是由Wnt信号介导的，这表明Wnt途径的激活对于再生的启动是必不可少的。结果表明，抑制PGE2的产生可以抑制Wnt激活并抑制上皮细胞和胚泡细胞的增殖。此外，我们的发现表明Wnt信号的强制激活可以挽救Cox拮抗剂对再生的抑制作用，表明PGE2通过非炎性机制对尾巴再生具有积极作用。结果表明，抑制PGE2的产生可以抑制Wnt激活并抑制上皮细胞和胚泡细胞的增殖。此外，我们的发现表明Wnt信号的强制激活可以挽救Cox拮抗剂对再生的抑制作用，表明PGE2通过非炎性机制对尾巴再生具有积极作用。结果表明，抑制PGE2的产生可以抑制Wnt激活并抑制上皮细胞和胚泡细胞的增殖。此外，我们的发现表明Wnt信号的强制激活可以挽救Cox拮抗剂对再生的抑制作用，表明PGE2通过非炎性机制对尾巴再生具有积极作用。