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作者

Hao Feng, Chunlei Tian, Wenshan Jiang, Zongxin Sun, Yikun Li, Baoshi Han, Lumei Chen, Dawei Wang, Hongjie Xiang, Jianchun Zhu, Wengang Song, Jingxin Li, Yunlu Cai, Shuanglian Wang, Yan Li

作者单位

Translational Medical Research Centre, the First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan, Shandong 250014, China. Electronic address: yli@email.sdfmu.edu.cn. Affiliations ¹ Department of Obstetrics & Gynecology, the First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan, Shandong 250014, China. ² Medical Science and Technology Innovation Center, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong 250012, China. ³ Department of Physiology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, China. ⁴ Institute of Women, Children and Reproductive Health, Shandong University, Jinan, Shandong 250012, China. ⁵ Central Laboratory, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan 250021, China. ⁶ Department of Traditional Chinese Medicine, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan, Shandong 250014, China. ⁷ Department of Pathology, the First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan, Shandong 250014, China. ⁸ Shandong Province University Clinical Immunology Translational Medicine Laboratory, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan, Shandong 250014, China. ⁹ Laboratory of Metabolism and Gastrointestinal Tumor, The First Affiliated Hospital of Shandong First Medical University& Shandong Provincial Qianfoshan Hospital, Jinan, Shandong 250014, China. ¹⁰ Medical Science and Technology Innovation Center, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong 250012, China. Electronic address: wsl6319@sdu.edu.cn. ¹¹ Shandong Province University Clinical Immunology Translational Medicine Laboratory, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan, Shandong 250014, China

刊名

International journal of biological macromolecules

年份

2025

卷号

Vol.299

页码

140240

ISSN

1879-0003

关键词

Hydrogen sulfide MTFR1L Mitochondria Persulfidation Trophoblast.

摘要

Hydrogen sulfide is bioactive in mammals. Reduced HS was observe in pregnancy complications, pre-eclampsia . Our previous data demonstrated that low dose of H2S enhanced cytotrophoblast invasion and migration via mitochondria dynamics without knowing the mechanisms. This study was designed to explore the functional regulation of CTB by mitochondrial fission regulator 1 like and the mechanisms. By studying human placenta samples and HTR-8/SVneo cell line, MTFR1L was found expressed in CTB. Whi...更多

Hydrogen sulfide is bioactive in mammals. Reduced HS was observe in pregnancy complications, pre-eclampsia . Our previous data demonstrated that low dose of H2S enhanced cytotrophoblast invasion and migration via mitochondria dynamics without knowing the mechanisms. This study was designed to explore the functional regulation of CTB by mitochondrial fission regulator 1 like and the mechanisms. By studying human placenta samples and HTR-8/SVneo cell line, MTFR1L was found expressed in CTB. While MTFR1L expression was lower in PE placenta and CTB comparing with Normal pregnancy. Knockdown of MTFR1L decreased CTB invasion and migration, as well as the ATP production, while increased the mitochondria fragmentation, ROS production and mitochondria membrane potential indicating MTFR1L was key regulator of mitochondria. The posttranslational modulation analysis showed enhanced persulfidation of MTFR1L on cystine 222 and 230 by HS. Mutations of MTFR1L suppressed ATP production, CTB invasion, migration, and increased mitochondria fragmentation, ROS production and mitochondria membrane potential. The present study showed the functional MTFR1L received endogenous CBS/H2S regulation. MTFR1L persulfidation by HS maintained mitochondria morphology and functions thus restored CTB invasion and migration. These findings established a new regulatory pathway for CTB invasion and migration, and provided new targets for PE treatment.收起

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