Volume 132, Issue 6 pp. 465-476
Original Article

The role of hsa_circ_0042260/miR-4782-3p/LAPTM4A axis in gestational diabetes mellitus

Rui Ji

Rui Ji

Department of Obstetrics, Xuyi People's Hospital, Huai'an, Jiangsu, China

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Hong Yang

Corresponding Author

Hong Yang

Department of Obstetrics, Xuyi People's Hospital, Huai'an, Jiangsu, China

Hong Yang, Department of Obstetrics, Xuyi People's Hospital, No. 28 Hongwu Avenue, Xuyu, Huai'an, Jiangsu 211700, China. e-mail: [email protected]

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Jiamei Chen

Jiamei Chen

Department of Obstetrics, Xuyi People's Hospital, Huai'an, Jiangsu, China

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Anna Zhao

Anna Zhao

Department of Obstetrics, Xuyi People's Hospital, Huai'an, Jiangsu, China

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Xia Chen

Xia Chen

Department of Obstetrics, Xuyi People's Hospital, Huai'an, Jiangsu, China

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Yanli Niu

Yanli Niu

Department of Obstetrics, Xuyi People's Hospital, Huai'an, Jiangsu, China

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First published: 08 April 2024

Abstract

Gestational diabetes mellitus (GDM) is a common metabolic condition during pregnancy, posing risks to both mother and fetus. CircRNAs have emerged as important players in various diseases, including GDM. We aimed to investigate the role of newly discovered circRNA, hsa_circ_0042260, in GDM pathogenesis. Using GSE194119 dataset, hsa_circ_0042260 was identified and its expression in plasma, placenta, and HG-stimulated HK-2 cells was examined. Silencing hsa_circ_0042260 in HK-2 cells assessed its impact on cell viability, apoptosis, and inflammation. Bioinformatics analysis revealed downstream targets of hsa_circ_0042260, namely miR-4782-3p and LAPTM4A. The interaction between hsa_circ_0042260, miR-4782-3p, and LAPTM4A was validated through various assays. hsa_circ_0042260 was upregulated in plasma from GDM patients and HG-stimulated HK-2 cells. Silencing hsa_circ_0042260 improved cell viability, suppressed apoptosis and inflammation. Hsa_circ_0042260 interacted with miR-4782-3p, which exhibited low expression in GDM patient plasma and HG-stimulated cells. MiR-4782-3p targeted LAPTM4A, confirmed by additional assays. LAPTM4A expression increased in GDM patient plasma and HG-induced HK-2 cells following hsa_circ_0042260 knockdown or miR-4782-3p overexpression. In rescue assays, inhibition of miR-4782-3p or overexpression of LAPTM4A counteracted the effects of hsa_circ_0042260 downregulation on cell viability, apoptosis, and inflammation. In conclusion, the hsa_circ_0042260/miR-4782-3p/LAPTM4A axis plays a role in regulating GDM progression in HG-stimulated HK-2 cells.

CONFLICT OF INTEREST STATEMENT

The authors have no conflict of interest.

DATA AVAILABILITY STATEMENT

The datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request.

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