Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, 226001, Jiangsu Province, China.
J Mol Histol. 2019 Dec;50(6):551-562. doi: 10.1007/s10735-019-09847-7. Epub 2019 Sep 18.
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.
尾巴再生是蜥蜴的一个显著特征;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物,在生理和病理条件下的炎症反应中已经得到了广泛的研究。PGE2 还通过与 Wnt 信号分子相互作用,作为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,PGE2 水平在尾巴再生的早期阶段增加,伴随着环氧化酶 1 和环氧化酶 2 的上调表达。接下来,我们证明了减少 PGE2 的产生会导致尾巴再生的延迟。随后的实验表明,这种效应可能是由 Wnt 信号介导的,这表明 Wnt 途径的激活对于再生的启动至关重要。结果表明,抑制 PGE2 的产生可以抑制 Wnt 的激活,并抑制上皮细胞和芽基细胞的增殖。此外,我们的研究结果表明,强制激活 Wnt 信号可以挽救 Cox 拮抗剂对再生的抑制作用,这表明 PGE2 通过非炎症机制对尾巴再生具有积极作用。