ArticleInternational journal of molecular sciences2019
Fetuin-A Inhibits Placental Cell Growth and Ciliogenesis in Gestational Diabetes Mellitus.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- The roles of centrosome amplification in diabetes-associated diseases.Frontiers in cell and developmental biology · 2026Article
- Article
- Fetuin-A Concentration in the Perinatal Period and Maternal BMI Dynamics During Pregnancy, Labor, and Early Postpartum: Is ΔBMI a Parameter Worth Considering?Journal of clinical medicine · 2025Article
- Prostaglandin E2 and Progesterone Receptor Coordinately Regulate Primary Cilia for Proper Decidualization.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Fetuin-A expression in human umbilical vein endothelial cells and amnion cells of patients with gestational diabetes mellitus.Saudi medical journal · 2022Article
- Disruption of Placental Homeostasis Leads to Preeclampsia.International journal of molecular sciences · 2020Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Gestational diabetes mellitus (GDM) is a type of unbalanced glucose tolerance that occurs during pregnancy, which affects approximately 10% of pregnancies worldwide. Fetuin-A is associated with insulin resistance, and the concentration of circulating fetuin-A increases in women with GDM, however, the role of fetuin-A in the placenta remains unclear. In this study, we enrolled placental samples from twenty pregnant women with GDM and twenty non-GDM pregnant women and found that the abundance of fetuin-A was upregulated in terms of mRNA and protein levels. Fetuin-A inhibited placental cell growth by inducing apoptosis and inhibiting S phase entry. Irregular alignment of mitotic chromosomes and aberrant mitotic spindle poles were observed. In addition, centrosome amplification was induced by fetuin-A treatment, and these amplified centrosomes nucleated microtubules with disorganized microtubule arrays in placental cells. Furthermore, fetuin-A inhibited autophagy, and thus blocked the growth of the primary cilium, a cellular antenna that regulates placenta development and differentiation. Thus, our study uncovered the novel function of fetuin-A in regulating placental cell growth and ciliogenesis.
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