期刊
BIOENGINEERED
卷 13, 期 3, 页码 5396-5406出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/21655979.2022.2036890
关键词
Asthma; miR-15b-5p; YAP1; ASM; proliferation; migration; ECM
资金
- Natural Science Foundation of China [81700030]
The miR-15b-5p/YAP1 axis regulates the proliferation, migration, inflammatory response, and ECM deposition of ASM cells in asthma.
The excessive proliferation and the deposition of extracellular matrix (ECM) of airway smooth muscle (ASM) cells facilitates airway remodeling in asthma. This study explores how microRNA-15b-5p (miR-15b-5p) functions in modulating the proliferation, migration, inflammatory response, and ECM deposition of ASM cells. MiR-15b-5p and yes-associated protein 1 (YAP1) mRNA expression levels in tumor necrosis factor alpha (TNF-alpha)-induced ASM cells were, respectively, examined by real-time quantitative polymerase-chain reaction. Besides, the proliferative ability and migrative potential of ASM cells were examined by cell counting kit-8 assay, 5-bromo-2 '-deoxyuridine assay, and transwell assays, respectively. Interleukin-6 and interleukin-8 levels in ASM cells were detected by enzyme-linked immunosorbent assay. YAP1, collagen I, and collagen III expressions in ASM cells were detected by Western blot. With dual-luciferase reporter gene assay, the relations between miR-15b-5p and YAP1 3MODIFIER LETTER PRIMEUTR in ASM cells was examined. MiR-15b-5p expression level was reduced in ASM cells treated with TNF-alpha. MiR-15b-5p repressed TNF-alpha-initiated growth and migration of ASM cells and also suppressed IL-6 and IL-8 secretion, and inhibited collagen I and collagen III expressions in ASM cells. Furthermore, it was validated that YAP1 was a downstream target of miR-15b-5p in ASM cells. Notably, YAP1 overexpression attenuated the inhibitory effects of miR-15b-5p up-regulation on the proliferation, migration, and inflammatory response, as well as ECM deposition of TNF-alpha-induced ASM cells. In conclusion, miR-15b-5p/YAP1 axis modulates the growth, migration, inflammatory response, and ECM deposition of ASM cells, thus participating in the pathogenesis of asthma.
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