GAS5 regulates viability and apoptosis in TGF-β1-stimulated bronchial epithelial cells by regulating miR-217/HDAC4 axis

Zhao Sihui; Ning Yunfang; Qin Na; Ping Nan; Yu Yong; Yin Guoyan

doi:10.1007/s13258-021-01092-1

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자료유형: 학술저널

저자정보: Zhao Sihui (Heping Hospital Affiliated to Changzhi Medical College) Ning Yunfang (Heping Hospital Affiliated to Changzhi Medical College) Qin Na (Heping Hospital Affiliated to Changzhi Medical College) Ping Nan (Heping Hospital Affiliated to Changzhi Medical College) Yu Yong (Heping Hospital Affiliated to Changzhi Medical College) Yin Guoyan (Heping Hospital Affiliated to Changzhi Medical College)

저널정보: 한국유전학회 Genes & Genomics Genes & Genomics Vol.43 No.8

발행연도: 2021.8

수록면: 837 - 846 (10page)

DOI: 10.1007/s13258-021-01092-1

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Background Asthma is a serious respiratory disease that afects the physical and mental health of children. Airway epithelial apoptosis concomitantly mediated by transforming growth factor-β1 (TGF-β1) is a crucial component of asthma pathogenesis. LncRNA growth Arrest Specifc 5 (GAS5), microRNA-217 (miR-217) and Histone deacetylase 4 (HDAC4) shown a close relationship with TGF-β1-induced injury of airway epithelial. However, the mechanism underlying TGF-β1-induced injury of airway epithelial in asthma still needs to be investigated. Objective We aimed to investigate the efect and underlying mechanism of GAS5/miR-217/HDAC4 axis in TGF-β1- stimulated bronchial epithelial cells. Methods The levels of were detected by quantitative real-time polymerase chain reaction (RT-qPCR). All protein levels were determined by western blot. Cell viability and apoptosis rate were assessed by Methyl thiazolyl tetrazolium (MTT) and Flow cytometry, respectively. The targeting relationship between miR-217 and GAS5 or HDAC4 was examined with dual-luciferase reporter assay. Results TGF-β1, GAS5, HDAC4 were up-regulated, while miR-217 was down-regulated in bronchial mucosal tissues of asthmatic children and TGF-β1-treated BEAS-2B cells. TGF-β1 could reduce cell viability and induce apoptosis, while these efects could be reversed by downregulation of GAS5 or HDAC4. Mechanically, GAS5 acted as a sponge for miR-217 to regulate the expression of HDAC4. Furthermore, overexpression of HDAC4 rescued the efects of GAS5 knockdown on viability and apoptosis of TGF-β1-induced BEAS-2B cells. GAS5 knockdown induced cell viability and hampered cell apoptosis in TGF-β1-stimulated BEAS-2B cells by regulating the miR-217/HDAC4 axis. Conclusions The lncRNA GAS5/miR-217/HDAC4 axis played an important role in regulating TGF-β1-induced bronchial epithelial cells injury, thus contributing to asthma.

#Asthma #TGF-β1 #GAS5 #MiR-217 #HDAC4

참고문헌 (23)

참고문헌 신청

Aysola RS / 2008 / Airway remodeling measured by multidetector CT is increased in severe asthma and correlates with pathology / Chest 134(6):1183~1191

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