TNFSF14, a novel target of miR‐326, facilitates airway remodeling in airway smooth muscle cells via inducing extracellular matrix protein deposition and proliferation
Abstract 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 inves...
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Wiley
2020-07-01
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| Series: | Kaohsiung Journal of Medical Sciences |
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| Online Access: | https://doi.org/10.1002/kjm2.12197 |
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doaj-d17ae05f7a9b44bcbe15fa8c014dcd092020-11-25T03:45:21ZengWileyKaohsiung Journal of Medical Sciences1607-551X2410-86502020-07-0136750851410.1002/kjm2.12197TNFSF14, a novel target of miR‐326, facilitates airway remodeling in airway smooth muscle cells via inducing extracellular matrix protein deposition and proliferationHui Zhang0Huan‐Li Yan1Xiang‐Yu Li2Yi‐Nan Guo3Department of Pediatric Affiliated Hospital of Changchun University of Chinese Medicine Changchun Jilin Province ChinaDepartment of Neonatology The Second People's Hospital of Liaocheng Liaocheng Shandong Province ChinaDepartment of Pediatric Affiliated Hospital of Changchun University of Chinese Medicine Changchun Jilin Province ChinaDepartment of Pediatric Affiliated Hospital of Changchun University of Chinese Medicine Changchun Jilin Province ChinaAbstract 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‐β1 (TGF‐β1) 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‐β1‐treated ASMCs. MiR‐326 mimics robustly decreased the collagen I and fibronectin levels and inhibited cell proliferation of TGF‐β1‐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‐β1‐treated ASMCs. In conclusion, miR‐326 suppressed matrix protein deposition and cell proliferation of TGF‐β1‐treated ASMCs via inhibiting TNFSF14. MiR‐326 might be a promising novel therapeutic target for asthma.https://doi.org/10.1002/kjm2.12197airway remodelingairway smooth muscle cellsasthmaextracellular matrix depositionmiR‐326TNFSF14 |
| collection |
DOAJ |
| language |
English |
| format |
Article |
| sources |
DOAJ |
| author |
Hui Zhang Huan‐Li Yan Xiang‐Yu Li Yi‐Nan Guo |
| spellingShingle |
Hui Zhang Huan‐Li Yan Xiang‐Yu Li Yi‐Nan Guo TNFSF14, a novel target of miR‐326, facilitates airway remodeling in airway smooth muscle cells via inducing extracellular matrix protein deposition and proliferation Kaohsiung Journal of Medical Sciences airway remodeling airway smooth muscle cells asthma extracellular matrix deposition miR‐326 TNFSF14 |
| author_facet |
Hui Zhang Huan‐Li Yan Xiang‐Yu Li Yi‐Nan Guo |
| author_sort |
Hui Zhang |
| title |
TNFSF14, a novel target of miR‐326, facilitates airway remodeling in airway smooth muscle cells via inducing extracellular matrix protein deposition and proliferation |
| title_short |
TNFSF14, a novel target of miR‐326, facilitates airway remodeling in airway smooth muscle cells via inducing extracellular matrix protein deposition and proliferation |
| title_full |
TNFSF14, a novel target of miR‐326, facilitates airway remodeling in airway smooth muscle cells via inducing extracellular matrix protein deposition and proliferation |
| title_fullStr |
TNFSF14, a novel target of miR‐326, facilitates airway remodeling in airway smooth muscle cells via inducing extracellular matrix protein deposition and proliferation |
| title_full_unstemmed |
TNFSF14, a novel target of miR‐326, facilitates airway remodeling in airway smooth muscle cells via inducing extracellular matrix protein deposition and proliferation |
| title_sort |
tnfsf14, a novel target of mir‐326, facilitates airway remodeling in airway smooth muscle cells via inducing extracellular matrix protein deposition and proliferation |
| publisher |
Wiley |
| series |
Kaohsiung Journal of Medical Sciences |
| issn |
1607-551X 2410-8650 |
| publishDate |
2020-07-01 |
| description |
Abstract 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‐β1 (TGF‐β1) 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‐β1‐treated ASMCs. MiR‐326 mimics robustly decreased the collagen I and fibronectin levels and inhibited cell proliferation of TGF‐β1‐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‐β1‐treated ASMCs. In conclusion, miR‐326 suppressed matrix protein deposition and cell proliferation of TGF‐β1‐treated ASMCs via inhibiting TNFSF14. MiR‐326 might be a promising novel therapeutic target for asthma. |
| topic |
airway remodeling airway smooth muscle cells asthma extracellular matrix deposition miR‐326 TNFSF14 |
| url |
https://doi.org/10.1002/kjm2.12197 |
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