MicroRNA-335-5p alleviates inflammatory response, airway fibrosis and autophagy in childhood asthma through targeted regulation of Autophagy related 5

Childhood Asthma is the most universal chronic disease, with significant cases reported. Despite the current progress in treatment, prognosis remain poor and the existing drugs cause serious side effects. This investigation explored the mechanisms and use of miR-335-5p on childhood asthma therapy. M...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Qingbin Liang, Jingjing He, Qian Yang, Qinghua Zhang, Yingjun Xu
Formato:	article
Lenguaje:	EN
Publicado:	Taylor & Francis Group 2021
Materias:	childhood asthma mir-335-5p atg5 inflammatory response airway fibrosis autophagy Biotechnology TP248.13-248.65
Acceso en línea:	https://doaj.org/article/89ba4ff3516e4a07b35548c484d987b8
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:89ba4ff3516e4a07b35548c484d987b8
record_format	dspace
spelling	oai:doaj.org-article:89ba4ff3516e4a07b35548c484d987b82021-11-04T15:51:54ZMicroRNA-335-5p alleviates inflammatory response, airway fibrosis and autophagy in childhood asthma through targeted regulation of Autophagy related 52165-59792165-598710.1080/21655979.2021.1996315https://doaj.org/article/89ba4ff3516e4a07b35548c484d987b82021-10-01T00:00:00Zhttp://dx.doi.org/10.1080/21655979.2021.1996315https://doaj.org/toc/2165-5979https://doaj.org/toc/2165-5987Childhood Asthma is the most universal chronic disease, with significant cases reported. Despite the current progress in treatment, prognosis remain poor and the existing drugs cause serious side effects. This investigation explored the mechanisms and use of miR-335-5p on childhood asthma therapy. MiR-335-5p and ATG5 expression was analyzed in clinical plasma samples through RT-qPCR. Airway smooth muscle cells (ASMCs) were cultured, and transfected with miR-335-5p mimic, miR-335-5p inhibitor, and pcDNA3.1-ATG5, or co-transfected with miR-335-5p mimic + pcDNA3.1-ATG5. Asthma cell models were constructed through TGF-β1, and animal models through ovalbumin (OVA). Monocyte-macrophage infiltration in bronchoalveolar lavage fluid (BALF) was determined by May−Grunwald−Giemsa staining, and collagen in lung tissue was assessed via Masson staining. Relationship between miR-335-5p and ATG5 was detected by Dual luciferase assay. Cell proliferation was detected by MTT assay. MiR-335-5p and ATG5 RNA expression was determined by RT-qPCR. Collagen I, collagen III, α-SMA, ATG5, LC3I/II, Beclin-1, and p62 protein expression levels in ASMCs was detected by western blot. MiR-335-5p expression was low, but ATG5 expression was high in childhood asthma. Versus OVA+ mimic NC group, the number of eosinophil and collagen in OVA+ miR-335-5p mimic group were reduced. In contrast to TGF-β1 + mimic NC group, TGF-β1 + miR-335-5p mimic group reduced inflammatory, airway fibrosis and autophagy in ASMCs. ATG5 was miR-335-5p target. Overexpressing ATG5 significantly reversed the inhibitory effects of miR-335-5p on inflammatory response, fibrosis and autophagy in ASMCs. Overall, the study concludes that MiR-335-5p alleviate inflammatory response, airway fibrosis and autophagy in childhood asthma through targeted regulation of ATG5.Qingbin LiangJingjing HeQian YangQinghua ZhangYingjun XuTaylor & Francis Grouparticlechildhood asthmamir-335-5patg5inflammatory responseairway fibrosisautophagyBiotechnologyTP248.13-248.65ENBioengineered, Vol 0, Iss 0 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	childhood asthma mir-335-5p atg5 inflammatory response airway fibrosis autophagy Biotechnology TP248.13-248.65
spellingShingle	childhood asthma mir-335-5p atg5 inflammatory response airway fibrosis autophagy Biotechnology TP248.13-248.65 Qingbin Liang Jingjing He Qian Yang Qinghua Zhang Yingjun Xu MicroRNA-335-5p alleviates inflammatory response, airway fibrosis and autophagy in childhood asthma through targeted regulation of Autophagy related 5
description	Childhood Asthma is the most universal chronic disease, with significant cases reported. Despite the current progress in treatment, prognosis remain poor and the existing drugs cause serious side effects. This investigation explored the mechanisms and use of miR-335-5p on childhood asthma therapy. MiR-335-5p and ATG5 expression was analyzed in clinical plasma samples through RT-qPCR. Airway smooth muscle cells (ASMCs) were cultured, and transfected with miR-335-5p mimic, miR-335-5p inhibitor, and pcDNA3.1-ATG5, or co-transfected with miR-335-5p mimic + pcDNA3.1-ATG5. Asthma cell models were constructed through TGF-β1, and animal models through ovalbumin (OVA). Monocyte-macrophage infiltration in bronchoalveolar lavage fluid (BALF) was determined by May−Grunwald−Giemsa staining, and collagen in lung tissue was assessed via Masson staining. Relationship between miR-335-5p and ATG5 was detected by Dual luciferase assay. Cell proliferation was detected by MTT assay. MiR-335-5p and ATG5 RNA expression was determined by RT-qPCR. Collagen I, collagen III, α-SMA, ATG5, LC3I/II, Beclin-1, and p62 protein expression levels in ASMCs was detected by western blot. MiR-335-5p expression was low, but ATG5 expression was high in childhood asthma. Versus OVA+ mimic NC group, the number of eosinophil and collagen in OVA+ miR-335-5p mimic group were reduced. In contrast to TGF-β1 + mimic NC group, TGF-β1 + miR-335-5p mimic group reduced inflammatory, airway fibrosis and autophagy in ASMCs. ATG5 was miR-335-5p target. Overexpressing ATG5 significantly reversed the inhibitory effects of miR-335-5p on inflammatory response, fibrosis and autophagy in ASMCs. Overall, the study concludes that MiR-335-5p alleviate inflammatory response, airway fibrosis and autophagy in childhood asthma through targeted regulation of ATG5.
format	article
author	Qingbin Liang Jingjing He Qian Yang Qinghua Zhang Yingjun Xu
author_facet	Qingbin Liang Jingjing He Qian Yang Qinghua Zhang Yingjun Xu
author_sort	Qingbin Liang
title	MicroRNA-335-5p alleviates inflammatory response, airway fibrosis and autophagy in childhood asthma through targeted regulation of Autophagy related 5
title_short	MicroRNA-335-5p alleviates inflammatory response, airway fibrosis and autophagy in childhood asthma through targeted regulation of Autophagy related 5
title_full	MicroRNA-335-5p alleviates inflammatory response, airway fibrosis and autophagy in childhood asthma through targeted regulation of Autophagy related 5
title_fullStr	MicroRNA-335-5p alleviates inflammatory response, airway fibrosis and autophagy in childhood asthma through targeted regulation of Autophagy related 5
title_full_unstemmed	MicroRNA-335-5p alleviates inflammatory response, airway fibrosis and autophagy in childhood asthma through targeted regulation of Autophagy related 5
title_sort	microrna-335-5p alleviates inflammatory response, airway fibrosis and autophagy in childhood asthma through targeted regulation of autophagy related 5
publisher	Taylor & Francis Group
publishDate	2021
url	https://doaj.org/article/89ba4ff3516e4a07b35548c484d987b8
work_keys_str_mv	AT qingbinliang microrna3355palleviatesinflammatoryresponseairwayfibrosisandautophagyinchildhoodasthmathroughtargetedregulationofautophagyrelated5 AT jingjinghe microrna3355palleviatesinflammatoryresponseairwayfibrosisandautophagyinchildhoodasthmathroughtargetedregulationofautophagyrelated5 AT qianyang microrna3355palleviatesinflammatoryresponseairwayfibrosisandautophagyinchildhoodasthmathroughtargetedregulationofautophagyrelated5 AT qinghuazhang microrna3355palleviatesinflammatoryresponseairwayfibrosisandautophagyinchildhoodasthmathroughtargetedregulationofautophagyrelated5 AT yingjunxu microrna3355palleviatesinflammatoryresponseairwayfibrosisandautophagyinchildhoodasthmathroughtargetedregulationofautophagyrelated5
_version_	1718444725738930176

MicroRNA-335-5p alleviates inflammatory response, airway fibrosis and autophagy in childhood asthma through targeted regulation of Autophagy related 5

Ejemplares similares