巨噬细胞促进损伤子宫内膜炎症的消退。

IF 5 2区 医学 Q2 CELL BIOLOGY
Jingman Li, Lijie Yin, Jiali Wang, Yuchen Pan, Chen Peng, Yue Dong, Sunan Shen, Yayi Hou, Guangfeng Zhao
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引用次数: 0

摘要

巨噬细胞在子宫内膜损伤的修复中发挥重要作用。虽然有报道称大腹膜巨噬细胞(lpm)可以迁移到受损器官并修复腹腔内的组织,但它们在修复受损子宫内膜中的作用尚不清楚。在这项研究中,我们使用了一种不涉及剖腹手术的子宫内膜损伤小鼠模型,这种手术通常会导致大量的lpm损失。引人注目的是,我们发现lpm在建模后6小时内到达子宫内膜。通过消耗或补充lpm,我们的研究结果表明,这些细胞能够吞噬子宫内膜中的死细胞并解决炎症。此外,我们观察到lpm的迁移效率随着小鼠17β-雌二醇(E2)水平的增加而增强。体外实验进一步证实E2可加速LPMs向凋亡的子宫内膜基质细胞迁移。总之,我们的研究结果表明,与E2水平相关,lpm迅速迁移到受损子宫内膜,并促进组织修复过程。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Large Peritoneal Macrophages Promote the Resolution of Inflammation in Injured Endometrium.

Macrophages play a significant role in the repair of endometrial injuries. While large peritoneal macrophages (LPMs) have been reported to migrate to injured organs and repair tissues within the peritoneal cavity, their involvement in the repair of injured endometrium remains unclear. In this study, we utilize a mouse model of endometrial injury that does not involve laparotomy, a procedure that typically results in a substantial loss of LPMs. Strikingly, we find that LPMs reach the endometrium within 6 h post-modeling. By depleting or supplementing LPMs, our results reveal that these cells are capable of engulfing dead cells in the endometrium and resolving inflammation. Additionally, we observe that the migration efficiency of LPMs is enhanced with increased levels of 17β-estradiol (E2) in mice. In vitro assays further confirm that E2 accelerates the migration of LPMs towards apoptotic endometrial stromal cells. Overall, our findings demonstrate that LPMs rapidly migrate into injured endometrium in relation to E2 levels and facilitate the process of tissue repair.

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来源期刊
Inflammation
Inflammation 医学-免疫学
CiteScore
9.70
自引率
0.00%
发文量
168
审稿时长
3.0 months
期刊介绍: Inflammation publishes the latest international advances in experimental and clinical research on the physiology, biochemistry, cell biology, and pharmacology of inflammation. Contributions include full-length scientific reports, short definitive articles, and papers from meetings and symposia proceedings. The journal''s coverage includes acute and chronic inflammation; mediators of inflammation; mechanisms of tissue injury and cytotoxicity; pharmacology of inflammation; and clinical studies of inflammation and its modification.
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