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LncRNA LOC103694972 promotes fibrosis of NRK-49F cells by regulating STAT3-dependent Smad/CTGF pathway via targeting miR-29c-3p

YAN LI1, HUZHI CAI2, XIAOLING PENG3, YOUHUI LIU4, QINGYANG CHEN4, XIANGDONG LIN5, XINYU CHEN6,*

1 Department of Vascular and Tumor Intervention, The First Hospital of Hunan University of Chinese Medicine, Changsha, 410007, China
2 Department of Intensive Care Unit, The First Hospital of Hunan University of Chinese Medicine, Changsha, 410007, China
3 Department of Nursing Research, The First Hospital of Hunan University of Chinese Medicine, Changsha, 410007, China
4 Department of Intensivie Care Unit, The First Hospital of Hunan University of Chinese Medicine, Changsha, 410007, China
5 Department of Endocrinology, The First Hospital of Hunan University of Chinese Medicine, Changsha, 410007, China
6 Department of Preventive Treatment Center, The First Hospital of Hunan University of Chinese Medicine, Changsha, 410007, China

* Corresponding Author: XINYU CHEN. Email: email

BIOCELL 2024, 48(3), 501-511. https://doi.org/10.32604/biocell.2023.030854

Abstract

Background: Renal fibrosis is an important process in the development of chronic kidney disease. Understanding the pathogenesis and finding effective treatments for renal fibrosis is crucial. This study aims to investigate whether a newly discovered long non-coding RNA (lncRNA) called LOC103694972 could be a potential target for treating fibrosis of NRK-49F cells. Methods:: LncRNA Chip was used to identify differentially expressed lncRNAs between TGF-β1-induced NRK-49F cells and normal cells. The dual-luciferase assay confirmed the binding between miR-29c-3p and signal transducer and activator of transcription (STAT3), as well as between miR-29c-3p and lncRNA LOC103694972. Si-LOC103694972 and miR-29c-3p mimic were then transfected into TGF-β1-induced NRK-49F cells. Results: The study found that LOC103694972 was highly expressed in TGF-β1-induced NRK-49F cells. These cells exhibited increased cell length and activity compared to the control group. The expression levels of Collagen I, α-Smooth muscle actin (α-SMA), and tissue inhibitor of metalloproteinase (TIMP-1) were increased, while matrix Metalloproteinase 2 (MMP2) and matrix Metalloproteinase 9 (MMP9) expression was decreased. However, transfection with si-LOC103694972 and miR-29c-3p mimics restored cell morphology and reduced cell viability. This led to a decrease in the levels of Collagen I, α-SMA, and TIMP-1, as well as an increase in MMP2 and MMP9 expression. Additionally, TGF-β1-induced NRK-49F cells transfected with miR-29c-3p mimics activated the STAT3-Smad3/CTGF pathway. Conclusion: Based on these findings, lncRNA LOC103694972 shows promise as a target for treating renal fibrosis. It negatively regulates miR-29c-3p and activates the STAT3-Smad3/CTGF pathway.

Graphical Abstract

LncRNA LOC103694972 promotes fibrosis of NRK-49F cells by regulating STAT3-dependent Smad/CTGF pathway via targeting miR-29c-3p

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APA Style
LI, Y., CAI, H., PENG, X., LIU, Y., CHEN, Q. et al. (2024). Lncrna LOC103694972 promotes fibrosis of NRK-49F cells by regulating stat3-dependent smad/ctgf pathway via targeting mir-29c-3p. BIOCELL, 48(3), 501-511. https://doi.org/10.32604/biocell.2023.030854
Vancouver Style
LI Y, CAI H, PENG X, LIU Y, CHEN Q, LIN X, et al. Lncrna LOC103694972 promotes fibrosis of NRK-49F cells by regulating stat3-dependent smad/ctgf pathway via targeting mir-29c-3p. BIOCELL . 2024;48(3):501-511 https://doi.org/10.32604/biocell.2023.030854
IEEE Style
Y. LI et al., "LncRNA LOC103694972 promotes fibrosis of NRK-49F cells by regulating STAT3-dependent Smad/CTGF pathway via targeting miR-29c-3p," BIOCELL , vol. 48, no. 3, pp. 501-511. 2024. https://doi.org/10.32604/biocell.2023.030854



cc This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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