研究动态
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Interleukin-33 通过丝裂原激活蛋白激酶信号通路促进小鼠子宫内粘连形成。

Interleukin-33 promotes intrauterine adhesion formation in mice through the mitogen-activated protein kinase signaling pathway.

发表日期:2024 Aug 20
作者: Dan Liu, Liwei Yuan, Fengjuan Xu, Yulan Ma, Huixing Zhang, Yiran Jin, Meixia Chen, Zhining Zhang, Sang Luo
来源: Stem Cell Research & Therapy

摘要:

IL-33属于炎症因子家族,与炎症反应密切相关。然而,其在宫腔粘连(IUAs)发展中的作用仍不清楚。在本研究中,将小鼠子宫内膜类器官移植到 IUA 小鼠模型中后,通过 RNA 测序鉴定了 IL-33 在子宫内膜损伤后 IUA 形成中的作用。 IL-33 治疗后,观察到小鼠子宫的主要病理变化,与纤维化标志物(如 TGF-β)的表达一致。这一发现可能归因于下游 MAPK 信号通路成分磷酸化的激活,这些成分是由巨噬细胞中 IL-33 的释放激活的。我们的研究提供了一种阐明 IUA 形成的新机制,为 IUA 的预防和临床治疗提出了新的治疗策略。© 2024。作者。
IL-33 belongs to the inflammatory factor family and is closely associated with the inflammatory response. However, its role in the development of intrauterine adhesions (IUAs) remains unclear. In this study, the role of IL-33 in the formation of IUAs after endometrial injury was identified via RNA sequencing after mouse endometrial organoids were transplanted into an IUA mouse model. Major pathological changes in the mouse uterus, consistent with the expression of fibrotic markers, such as TGF-β, were observed in response to treatment with IL-33. This finding may be attributed to activation of the phosphorylation of downstream MAPK signaling pathway components, which are activated by the release of IL-33 in macrophages. Our study provides a novel mechanism for elucidating IUA formation, suggesting a new therapeutic strategy for the prevention and clinical treatment of IUAs.© 2024. The Author(s).