Fine particulate matter (PM2.5) induces microRNA-192–5p causing glomerular damage

Yarbakht M, Sarau G, Xu Y, Fang X, Mirzaei Z, Krüger R, Xiao Y, Usman A, Daniel C, Schiffer M, Christiansen S, Müller-Deile J (2025)

Publication Type: Journal article

Publication year: 2025

Journal

Ecotoxicology and Environmental Safety Elsevier

Book Volume: 298

Article Number: 118280

DOI: 10.1016/j.ecoenv.2025.118280

Abstract

An association between air pollution and the incidence of membranous glomerulonephritis (MGN) has been shown in epidemiological studies. However, the causality of this relationship and data on potential pathomechanisms are still missing. Anti-phospholipase A2 receptor (PLA2R1) antibodies, upregulation of microRNA-192–5p, and decreased expression of its podocyte target nephronectin (NPNT) in patients with MGN have been shown, but the trigger for these regulations remained unknown. The current study aimed to assay the possible role of PM2.5 in the pathogenesis of MGN. In this study, we characterized particulate matter (PM2.5) collected on air filters in Shanghai by scanning electron microscopy, energy dispersive X-ray spectroscopy, X-ray fluorescence, microwave plasma atomic emission spectroscopy, nanoparticle tracking analysis, and Raman spectroscopy. Cultured human podocytes, zebrafish, and mice were exposed to PM2.5 to assess possible effects on glomerular function and ultrastructure. PM2.5 caused a reduction of podocyte-specific markers and upregulation of microRNA-192–5p. Moreover, NPNT/npnt/Npnt were downregulated, while PLA2R1/pla2r1/Pla2r1 were upregulated. PM2.5 was able to cause edema, proteinuria, and glomerular damage with loosening of the glomerular basement membrane and partial podocyte effacement in zebrafish larvae. BulkRNA seq analysis and qPCR of zebrafish larvae showed an increase in inflammatory response and oxidative stress due to the exposure to PM2.5. Long-term exposure of mice to ambient PM2.5 induced glomerular damage, albuminuria, and upregulation of pulmonary microRNA-192–5p. Therefore, air pollution might be involved in developing MGN through inflammatory pathways and the induction of microRNA-192–5p, which targets gene expression important for glomerular cell function.

Authors with CRIS profile

Melina Yarbakht Department of Medicine 4 – Nephrology and Hypertension René Krüger Department of Medicine 4 – Nephrology and Hypertension Christoph Daniel Department of Nephropathology Mario Schiffer Lehrstuhl für Innere Medizin IV Janina Müller-Deile Department of Medicine 4 – Nephrology and Hypertension

Involved external institutions

Fraunhofer-Institut für Keramische Technologien und Systeme (IKTS) DE Germany (DE) Fudan University / 复旦大学 CN China (CN) Innovations-Institut für Nanotechnologie und korrelative Mikroskopie e.V. (INAM) / Institute for Nanotechnology and Correlative Microscopy DE Germany (DE)

How to cite

APA:

Yarbakht, M., Sarau, G., Xu, Y., Fang, X., Mirzaei, Z., Krüger, R.,... Müller-Deile, J. (2025). Fine particulate matter (PM2.5) induces microRNA-192–5p causing glomerular damage. Ecotoxicology and Environmental Safety, 298. https://doi.org/10.1016/j.ecoenv.2025.118280

MLA:

Yarbakht, Melina, et al. "Fine particulate matter (PM2.5) induces microRNA-192–5p causing glomerular damage." Ecotoxicology and Environmental Safety 298 (2025).

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