Journal
KAOHSIUNG JOURNAL OF MEDICAL SCIENCES
Volume 36, Issue 7, Pages 508-514Publisher
WILEY
DOI: 10.1002/kjm2.12197
Keywords
airway remodeling; airway smooth muscle cells; asthma; extracellular matrix deposition; miR-326; TNFSF14
Categories
Ask authors/readers for more resources
As a common chronic respiratory disease, the incidence of asthma is increasing in recent years worldwide. Airway remodeling is the primary pathological basis of refractory asthma, but the studies about the underlying mechanism of airway remodeling was a lack. In the study, we aimed to investigate the effects and mechanisms of miR-326 on airway remodeling in airway smooth muscle cells (ASMCs). The results showed that transforming growth factor-beta 1 (TGF-beta 1) accelerated matrix protein deposition by increasing the expression levels of collagen I and fibronectin, and promoted proliferative ability of ASMCs. However, miR-326 was significantly downregulated in TGF-beta 1-treated ASMCs. MiR-326 mimics robustly decreased the collagen I and fibronectin levels and inhibited cell proliferation of TGF-beta 1-treated ASMCs. Luciferase assay investigated that tumor necrosis factor superfamily member 14 (TNFSF14) was a direct target of miR-326. The expression of TNFSF14 was negatively regulated by miR-326. Moreover, exogenous TNFSF14 effectively reversed the inhibitory effects of miR-326 overexpression on the expression levels of collagen I and fibronectin, and promoted cell proliferation of TGF-beta 1-treated ASMCs. In conclusion, miR-326 suppressed matrix protein deposition and cell proliferation of TGF-beta 1-treated ASMCs via inhibiting TNFSF14. MiR-326 might be a promising novel therapeutic target for asthma.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available