miR-212-5p Regulates PM2.5-Induced Apoptosis by Targeting LAMC2 and LAMA3

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(4), P. 1761 - 1761

Published: Feb. 19, 2025

Fine particulate matter (PM2.5) is often linked to a range of respiratory diseases and cellular damage. Although studies have shown that the expression profiles microRNAs (miRNAs) are altered during lung damage brought on by PM2.5, underlying functions miRNAs remain poorly understood. In this research, we explored role PM2.5-induced apoptosis in detail focused miRNA (miR-212-5p) regulates apoptosis. Through dual-luciferase assay, direct targeting connection between laminin subunits γ2 (LAMC2) α3 (LAMA3) miR-212-5p was successfully demonstrated. This study revealing negative regulatory relationship LAMC2 LAMA3, providing important clues for deeper understanding relevant physiological pathological mechanisms. The present showed LAMA3 positively regulate PI3K-AKT pathway negatively NF-κB pathway, which directly leads significant changes rates. reveals previously unrecognized molecular mechanism showing targets thus associates with via PI3K/AKT/NF-κB pathway. These findings not only redefine but also open up new avenues future research.

Language: Английский

Airway epithelial cells as drivers of severe asthma pathogenesis

Mucosal Immunology, Journal Year: 2025, Volume and Issue: unknown

Published: March 1, 2025

Our understanding of the airway epithelium's role in driving asthma pathogenesis has evolved over time. From being regarded primarily as a physical barrier that could be damaged via inflammation, epithelium is now known to actively contribute development through interactions with immune system. The contains multiple cell types specialized functions spanning action, mucociliary clearance, recruitment, and maintenance tissue homeostasis. Environmental insults may cause direct or indirect injury leading impaired function, epithelial remodelling increased release inflammatory mediators. In severe asthma, repair process inhibited response exaggerated, downstream inflammation. Genetic epigenetic mechanisms also maintain dysregulation barrier, adding disease chronicity. Here, we review how targeting can treatment.

Language: Английский

Plasma exosomes from patients with coronary artery disease promote atherosclerosis via impairing vascular endothelial junctions

Scientific Reports, Journal Year: 2024, Volume and Issue: 14(1)

Published: Nov. 30, 2024

The underlying mechanism of vascular endothelial hyperpermeability caused by decrease junctions occurring in atherosclerosis remains elusive. Our findings identified that plasma exosomes from patients with stable coronary artery disease (ExoSCAD) contain differentially expressed miRNAs are clustered genes related to cell junctions, prompting us investigate the role ExoSCAD regulating and elucidate mechanisms. Here, we show markedly impair via suppressing VE-Cadherin ZO-1 cells vitro vivo, consequently increases permeability. Critically, exosomal miR-140-3p plays a crucial ExoSCAD-induced inhibition ZO-1, may be an important causative factor development during atherosclerosis. Additionally, miR-140–3p level coordinates severity SCAD. Targeting circulating might open novel options for treatment

Language: Английский