Open Access

ARTICLE

Biological function of miRNA-145-5p in angiotensin II induced renal inflammation

by BIN LI^1,2,3,#, YUCHENG SHENG^4,#, XIAOYING XU⁴, SHENGCUN WANG³, HONGYAN SONG³, JINGYUAN LI³, HAONAN JI¹, QINGHUA WANG³, XIAODI ZHOU^1,*, LONGJU QI^2,*

1 Department of Pediatrics, Affiliated Hospital of Nantong University, Nantong, 226001, China
2 Department of Science and Education, Affiliated Nantong Hospital 3 of Nantong University, Nantong, 226001, China
3 Laboratory Animal Center, Nantong University, Nantong, 226001, China
4 Department of Gynecology and Obstetrics and Department of Oncology, Hai’an Hospital Affiliated to Nantong University, Nantong, 226600, China

* Corresponding Authors: XIAODI ZHOU. Email: ; LONGJU QI. Email:
# These authors contributed equally to this work

BIOCELL 2024, 48(4), 601-611. https://doi.org/10.32604/biocell.2024.047404

Received 04 November 2023; Accepted 20 February 2024; Issue published 09 April 2024

Abstract

Objective: Chronic kidney disease (CKD) is a progressive disorder characterized by intricate structural and functional alterations in the kidneys, attributable to diverse causative factors. Notably, the therapeutic promise of miR-145-5p in addressing renal pathologies has been discerned. This investigation seeks to elucidate the functional role of miR-145-5p in injured kidneys by subjecting human glomerular mesangial cells (HGMCs) to stimulation with Angiotensin II (AngII). Materials and Methods: Cellular viability and the levels of inflammatory mediators were evaluated utilizing Cell Counting Kit-8 (CCK-8), quantitative real-time polymerase chain reaction (qRT-PCR), and western blot methodologies, both in the presence of AngII incubation and in scenarios of miR-145p overexpression and downregulation. Furthermore, the cell cycle dynamics were elucidated through Fluorescence-activated Cell Sorting (FACS) analysis. Results: AngII incubation induced an upregulation of miR-145-5p and inflammatory factors including Intercellular Adhesion Molecule 1 (ICAM-1), Interleukin 6 (IL-6), Interleukin 8 (IL-8), and Interleukin 1β (IL-1β). Additionally, it elevated the expression of Cyclin A2, Cyclin D1, and the G2/M cell cycle ratio. Conversely, inhibition of miR-145-5p heightened the levels of inflammatory factors and cell cycle regulators induced by AngII incubation. Reduced expression of miR-145-5p correlated with a downregulation of Interleukin 10 (IL-10) expression, concurrently promoting HGMC proliferation under AngII stimulation. Moreover, ectopic miR-145-5p expression demonstrated a reduction in inflammatory factors, cell cyclin regulators, G2/M cell cycle ratio, and overall proliferation. Conclusion: MiR-145-5p exhibited inhibitory effects on the inflammatory response and proliferation induced by Angiotensin II in HGMCs, showcasing its potential as a therapeutic avenue for the treatment of kidney injury.

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Keywords

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