LncRNA GAS5 participates in childhood pneumonia by inhibiting cell apoptosis and promoting SHIP-1 expression via downregulating miR-155

Abstract Background LncRNA GAS5 and miR-155 are reported to play opposite roles in lung inflammatory responses. Lung inflammation participates in childhood pneumonia, indicating the involvement of GAS5 and miR-155 in pneumonia. The study aimed to analyze the potential interaction between GAS5 and mi...

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Autores principales:	Xiaoping Wang, Ping Guo, Jiahui Tian, Jie Li, Na Yan, Xin Zhao, Yue Ma
Formato:	article
Lenguaje:	EN
Publicado:	BMC 2021
Materias:	GAS5 Childhood pneumonia miR-155 Apoptosis SHIP-1 Methylation Diseases of the respiratory system RC705-779
Acceso en línea:	https://doaj.org/article/6a614dc3608a475fade59500d62a40b1
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spelling	oai:doaj.org-article:6a614dc3608a475fade59500d62a40b12021-11-14T12:37:22ZLncRNA GAS5 participates in childhood pneumonia by inhibiting cell apoptosis and promoting SHIP-1 expression via downregulating miR-15510.1186/s12890-021-01724-y1471-2466https://doaj.org/article/6a614dc3608a475fade59500d62a40b12021-11-01T00:00:00Zhttps://doi.org/10.1186/s12890-021-01724-yhttps://doaj.org/toc/1471-2466Abstract Background LncRNA GAS5 and miR-155 are reported to play opposite roles in lung inflammatory responses. Lung inflammation participates in childhood pneumonia, indicating the involvement of GAS5 and miR-155 in pneumonia. The study aimed to analyze the potential interaction between GAS5 and miR-155 in childhood pneumonia. Methods GAS5 and miR-155 levels in plasma samples from pneumonia patients and controls were detected using RT-qPCR. The role of GAS5 in miR-155 RNA gene methylation in human bronchial epithelial cells (HBEpCs) was analyzed by methylation analysis. Flow cytometry and RT-qPCR were applied to analyze cell apoptosis and SHIP-1 expression, respectively. Results GAS5 was downregulated in pneumonia, and miR-155 was upregulated in pneumonia. GAS5 and miR-155 were inversely correlated. GAS5 overexpression decreased miR-155 expression in HBEpCs, while miR-155 overexpression showed no significant effects on GAS5 expression. In addition, GAS5 suppressed LPS-induced HBEpC apoptosis, promoted SHIP-1 expression, and reduced the enhancing effect of miR-155 on cell apoptosis and SHIP-1 expression. Conclusions GAS5 may participate in childhood pneumonia by inhibiting cell apoptosis and promoting SHIP-1 expression via downregulating miR-155.Xiaoping WangPing GuoJiahui TianJie LiNa YanXin ZhaoYue MaBMCarticleGAS5Childhood pneumoniamiR-155ApoptosisSHIP-1MethylationDiseases of the respiratory systemRC705-779ENBMC Pulmonary Medicine, Vol 21, Iss 1, Pp 1-9 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	GAS5 Childhood pneumonia miR-155 Apoptosis SHIP-1 Methylation Diseases of the respiratory system RC705-779
spellingShingle	GAS5 Childhood pneumonia miR-155 Apoptosis SHIP-1 Methylation Diseases of the respiratory system RC705-779 Xiaoping Wang Ping Guo Jiahui Tian Jie Li Na Yan Xin Zhao Yue Ma LncRNA GAS5 participates in childhood pneumonia by inhibiting cell apoptosis and promoting SHIP-1 expression via downregulating miR-155
description	Abstract Background LncRNA GAS5 and miR-155 are reported to play opposite roles in lung inflammatory responses. Lung inflammation participates in childhood pneumonia, indicating the involvement of GAS5 and miR-155 in pneumonia. The study aimed to analyze the potential interaction between GAS5 and miR-155 in childhood pneumonia. Methods GAS5 and miR-155 levels in plasma samples from pneumonia patients and controls were detected using RT-qPCR. The role of GAS5 in miR-155 RNA gene methylation in human bronchial epithelial cells (HBEpCs) was analyzed by methylation analysis. Flow cytometry and RT-qPCR were applied to analyze cell apoptosis and SHIP-1 expression, respectively. Results GAS5 was downregulated in pneumonia, and miR-155 was upregulated in pneumonia. GAS5 and miR-155 were inversely correlated. GAS5 overexpression decreased miR-155 expression in HBEpCs, while miR-155 overexpression showed no significant effects on GAS5 expression. In addition, GAS5 suppressed LPS-induced HBEpC apoptosis, promoted SHIP-1 expression, and reduced the enhancing effect of miR-155 on cell apoptosis and SHIP-1 expression. Conclusions GAS5 may participate in childhood pneumonia by inhibiting cell apoptosis and promoting SHIP-1 expression via downregulating miR-155.
format	article
author	Xiaoping Wang Ping Guo Jiahui Tian Jie Li Na Yan Xin Zhao Yue Ma
author_facet	Xiaoping Wang Ping Guo Jiahui Tian Jie Li Na Yan Xin Zhao Yue Ma
author_sort	Xiaoping Wang
title	LncRNA GAS5 participates in childhood pneumonia by inhibiting cell apoptosis and promoting SHIP-1 expression via downregulating miR-155
title_short	LncRNA GAS5 participates in childhood pneumonia by inhibiting cell apoptosis and promoting SHIP-1 expression via downregulating miR-155
title_full	LncRNA GAS5 participates in childhood pneumonia by inhibiting cell apoptosis and promoting SHIP-1 expression via downregulating miR-155
title_fullStr	LncRNA GAS5 participates in childhood pneumonia by inhibiting cell apoptosis and promoting SHIP-1 expression via downregulating miR-155
title_full_unstemmed	LncRNA GAS5 participates in childhood pneumonia by inhibiting cell apoptosis and promoting SHIP-1 expression via downregulating miR-155
title_sort	lncrna gas5 participates in childhood pneumonia by inhibiting cell apoptosis and promoting ship-1 expression via downregulating mir-155
publisher	BMC
publishDate	2021
url	https://doaj.org/article/6a614dc3608a475fade59500d62a40b1
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LncRNA GAS5 participates in childhood pneumonia by inhibiting cell apoptosis and promoting SHIP-1 expression via downregulating miR-155

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