IGFBP1抑制HTR-8/SVneo滋养细胞在子痫前期的侵袭、迁移和凋亡。

IF 1.5 4区医学 Q3 OBSTETRICS & GYNECOLOGY

Hypertension in Pregnancy Pub Date : 2022-02-01 Epub Date: 2022-02-16 DOI:10.1080/10641955.2022.2033259

Xiujuan Li, Chenxi Li, Ye Wang, Jianxing Cai, Li Zhao, Zhiying Su, Huiming Ye

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引用次数: 4

摘要

目的:探讨IGFBP1对模拟子痫前期滋养细胞生物学功能的影响及其机制。方法:采用免疫组化方法检测IGFBP1在胎盘组织中的表达。以igfbp1过表达和缺氧复氧刺激HTR-8/SVneo细胞，分别用CCK8、transwell和流式细胞术检测细胞增殖、侵袭、迁移和凋亡情况。结果:IGFBP1在子痫前期胎盘中表达升高。IGFBP1过表达可抑制HTR-8/SVneo细胞的增殖、侵袭、迁移和凋亡，并诱导MMP-26在缺氧再氧化或无缺氧再氧化条件下的表达。结论:IGFBP1影响滋养细胞的生物学功能，可能通过诱导MMP-26参与子痫前期的病理生理。

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IGFBP1 inhibits the invasion, migration, and apoptosis of HTR-8/SVneo trophoblast cells in preeclampsia.

Objective: To investigate the effects and underlying mechanisms of IGFBP1 on the biological functions of trophoblasts in simulated preeclampsia.

Methods: IGFBP1 expression in placenta was determined by immunohistochemistry. HTR-8/SVneo cells were stimulated with/without IGFBP1-overexpression and hypoxia-reoxygenation, and the proliferation, invasion, migration, and apoptosis were detected by CCK8, transwell, and flow cytometry, respectively.

Results: IGFBP1 expression was increased in placenta of preeclampsia. IGFBP1 overexpression inhibited proliferation, invasion, migration, and apoptosis of HTR-8/SVneo cells and induced MMP-26 expression with/without hypoxia-reoxygenation challenge.

Conclusion: IGFBP1 affects biological functions of trophoblasts, and it may play a role in pathophysiology of preeclampsia by inducing MMP-26.

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来源期刊

Hypertension in Pregnancy 医学-妇产科学

CiteScore

3.40

自引率

0.00%

发文量

审稿时长

6 months

期刊介绍： Hypertension in Pregnancy is a refereed journal in the English language which publishes data pertaining to human and animal hypertension during gestation. Contributions concerning physiology of circulatory control, pathophysiology, methodology, therapy or any other material relevant to the relationship between elevated blood pressure and pregnancy are acceptable. Published material includes original articles, clinical trials, solicited and unsolicited reviews, editorials, letters, and other material deemed pertinent by the editors.