Trophoblast fusion in fetal growth restriction is inhibited by CTGF in a cell-cycle-dependent manner

IF 2.9 4区生物学 Q3 CELL BIOLOGY

Journal of Molecular Histology Pub Date : 2024-08-10 DOI:10.1007/s10735-024-10239-9

Ketong Liu, Suwen Wu, Yutong Cui, Xiang Tao, Yanhong Li, Xirong Xiao

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Abstract

Fetal growth restriction (FGR) is a relatively common complication of pregnancy, and insufficient syncytialization in the placenta may play an important role in the pathogenesis of FGR. However, the mechanism of impaired formation of the syncytiotrophoblast layer in FGR patients requires further exploration. In the present study, we demonstrated that the level of syncytialization was decreased in FGR patient placentas, while the expression of connective tissue growth factor (CTGF) was significantly upregulated. CTGF was found to inhibit trophoblast fusion via regulating cell cycle progress of BeWo cells. Furthermore, we found that CTGF negatively regulates cell cycle arrest in a p21-dependent manner as overexpression of p21 could rescue the impaired syncytialization induced by CTGF-overexpression. Besides, we also identified that CTGF inhibits the expression of p21 through ITGB4/PI3K/AKT signaling pathway. Our study provided a new insight for elucidating the pathogenic mechanism of FGR and a novel idea for the clinical therapy of FGR.

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CTGF以细胞周期依赖性方式抑制胎儿生长受限时滋养细胞的融合。

胎儿生长受限（FGR）是一种比较常见的妊娠并发症，胎盘合胞化不足可能在FGR的发病机制中起着重要作用。然而，FGR 患者合胞滋养层形成障碍的机制还需要进一步探讨。在本研究中，我们发现FGR患者胎盘的合胞化水平降低，而结缔组织生长因子（CTGF）的表达显著上调。研究发现，CTGF 可通过调节 BeWo 细胞的细胞周期进程抑制滋养细胞融合。此外，我们还发现 CTGF 以 p21 依赖性方式负向调控细胞周期停滞，因为过表达 p21 可挽救 CTGF 过表达诱导的合胞化受损。此外，我们还发现 CTGF 通过 ITGB4/PI3K/AKT 信号通路抑制 p21 的表达。我们的研究为阐明FGR的致病机制提供了新的见解，也为FGR的临床治疗提供了新的思路。

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来源期刊

Journal of Molecular Histology 生物-细胞生物学

CiteScore

5.90

自引率

0.00%

发文量

审稿时长

1 months

期刊介绍： The Journal of Molecular Histology publishes results of original research on the localization and expression of molecules in animal cells, tissues and organs. Coverage includes studies describing novel cellular or ultrastructural distributions of molecules which provide insight into biochemical or physiological function, development, histologic structure and disease processes. Major research themes of particular interest include: - Cell-Cell and Cell-Matrix Interactions; - Connective Tissues; - Development and Disease; - Neuroscience. Please note that the Journal of Molecular Histology does not consider manuscripts dealing with the application of immunological or other probes on non-standard laboratory animal models unless the results are clearly of significant and general biological importance. The Journal of Molecular Histology publishes full-length original research papers, review articles, short communications and letters to the editors. All manuscripts are typically reviewed by two independent referees. The Journal of Molecular Histology is a continuation of The Histochemical Journal.