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不同来源不明原因复发性自然流产患者母胎界面中高迁移率族蛋白 B1 水平上调。

Upregulated HMGB1 levels in maternal-fetal interface of patients with unexplained recurrent spontaneous abortion from different sources.

机构信息

Department of Obstetrics and Gynecology, Reproductive Medicine Center, The First Affiliated Hospital of Anhui Medical University, Hefei, China.

NHC Key Laboratory of Study on Abnormal Gametes and Reproductive Tract (Anhui Medical University), Hefei, China.

出版信息

J Matern Fetal Neonatal Med. 2022 Dec;35(25):6542-6549. doi: 10.1080/14767058.2021.1918084. Epub 2021 May 4.

DOI:10.1080/14767058.2021.1918084
PMID:33944653
Abstract

OBJECTIVE

To investigate the expression and sources of high mobility group box 1 (HMGB1) protein in the maternal-fetal interface of patients with unexplained recurrent spontaneous abortion (URSA), and further to verify the role of HMGB1 in the etiology of URSA.

METHODS

55 women at early pregnancy with URSA and 55 women undergoing selective termination of normal early pregnancy as control were included. The abortion tissues including villi and decidua were collected. The expression of HMGB1, CD45, CK7, and vimentin in abortion tissues was detected, and the localization and sources of HMGB1 were analyzed.

RESULTS

Infiltrating immune cells and expression of HMGB1 were significantly increased in villi and decidua in URSA group compared with those in the control group. In the URSA group, HMGB1 was colocalized with the CD45-labeled immune cells, and it was more obvious in decidua than in villi; in addition, HMGB1 was colocalized with the vimentin-labeled decidual stromal cells, but not with the CK7- labeled villous epithelial cells.

CONCLUSION

High expression of HMGB1 in the maternal-fetal interface in URSA patients was actively secreted by the infiltrating immune cells, and decidual stromal cells may passively release HMGB1 during necrosis.

摘要

目的

探讨不明原因复发性自然流产(URSA)患者母体-胎儿界面高迁移率族蛋白 1(HMGB1)蛋白的表达和来源,进一步验证 HMGB1 在 URSA 发病机制中的作用。

方法

纳入 55 例 URSA 早孕患者和 55 例选择性终止正常早孕患者作为对照。收集流产组织,包括绒毛和蜕膜。检测流产组织中 HMGB1、CD45、CK7 和波形蛋白的表达,分析 HMGB1 的定位和来源。

结果

URSA 组绒毛和蜕膜中浸润的免疫细胞和 HMGB1 的表达明显高于对照组。在 URSA 组中,HMGB1 与 CD45 标记的免疫细胞共定位,在蜕膜中比在绒毛中更明显;此外,HMGB1 与 vimentin 标记的蜕膜基质细胞共定位,但与 CK7 标记的绒毛上皮细胞不共定位。

结论

URSA 患者母体-胎儿界面 HMGB1 的高表达是由浸润的免疫细胞主动分泌的,而蜕膜基质细胞在坏死过程中可能被动释放 HMGB1。

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