TY - JOUR
T1 - Fetuin-A inhibits placental cell growth and ciliogenesis in gestational diabetes mellitus
AU - Wang, Chia Yih
AU - Su, Mei Tsz
AU - Cheng, Hui Ling
AU - Kuo, Pao Lin
AU - Tsai, Pei Yin
N1 - Funding Information:
Funding: This study was supported by grants from the Ministry of Science and Technology, MOST106-2320-B-006-056-MY3 to Chia-Yih Wang and MOST107-2314-B-006-042 to Pei-Yin Tsai. This study was supported by a grant from the National Cheng Kung University Hospital, NCKUH-10505024 to Pei-Yin Tsai.
Funding Information:
Acknowledgments: We are grateful for the support from the Core Research Laboratory, College of Medicine, National Cheng Kung University.
Funding Information:
This study was supported by grants from the Ministry of Science and Technology, MOST 106-2320-B-006-056-MY3 to Chia-Yih Wang and MOST 107-2314-B-006-042 to Pei-Yin Tsai. This study was supported by a grant from the National Cheng Kung University Hospital, NCKUH-10505024 to Pei-Yin Tsai.
Publisher Copyright:
© 2019 by the authors. Licensee MDPI, Basel, Switzerland.
PY - 2019/10
Y1 - 2019/10
N2 - 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.
AB - 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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U2 - 10.3390/ijms20205207
DO - 10.3390/ijms20205207
M3 - Article
C2 - 31640125
AN - SCOPUS:85073751470
VL - 20
JO - International Journal of Molecular Sciences
JF - International Journal of Molecular Sciences
SN - 1661-6596
IS - 20
M1 - 5207
ER -