Expression profile of lncRNA in human bronchial epithelial cells response to Talaromyces marneffei infection: A microarray analysis

2017 ◽  
Vol 104 ◽  
pp. 155-160 ◽  
Author(s):  
Yinghua Li ◽  
Meihua Li ◽  
Honglin Luo ◽  
Jing Bai ◽  
Jianquan Zhang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Microarray Analysis ◽  
Expression Profile ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Talaromyces Marneffei

scholarly journals Microarray analysis uncovers retinoid targets in human bronchial epithelial cells

Oncogene ◽  
2003 ◽  
Vol 22 (31) ◽  
pp. 4924-4932 ◽  
Author(s):  
Yan Ma ◽  
Petra H Koza-Taylor ◽  
Debra A DiMattia ◽  
Lynn Hames ◽  
Haoning Fu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Microarray Analysis ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial

GENE EXPRESSION PROFILE BY RNAi-MEDIATED SUPPRESSION OF S100A2 IN HUMAN BRONCHIAL EPITHELIAL CELLS

Toukeibu Gan ◽  
2005 ◽  
Vol 31 (4) ◽  
pp. 481-486
Author(s):  
Nobuhiko ORIDATE ◽  
Takatsugu MIZUMACHI ◽  
Fumiyuki SUZUKI ◽  
Akihiro HOMMA ◽  
Yasushi FURUTA ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial

scholarly journals Gene Expression Profile and Toxic Effects in Human Bronchial Epithelial Cells Exposed to Zearalenone

PLoS ONE ◽  
2014 ◽  
Vol 9 (5) ◽  
pp. e96404 ◽  
Author(s):  
Mei Yu So ◽  
ZhiPeng Tian ◽  
Yong Shian Phoon ◽  
Sha Sha ◽  
Michael N. Antoniou ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Bronchial Epithelial Cells ◽  
Toxic Effects ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial

scholarly journals Identification of abnormally expressed lncRNAs induced by PM2.5 in human bronchial epithelial cells

2018 ◽  
Vol 38 (5) ◽  
Author(s):  
Xing Li ◽  
Mengning Zheng ◽  
Jinding Pu ◽  
Yumin Zhou ◽  
Wei Hong ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Western Blot ◽  
Mrna Expression ◽  
Microarray Analysis ◽  
Cell Apoptosis ◽  
Expression Profiles ◽  
Bronchial Epithelial Cells ◽  
Dependent Manner ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial

To investigate the effect of stimulation of human bronchial epithelial cells (HBECs) by arterial traffic ambient PM2.5 (TAPM2.5) and wood smoke PM2.5 (WSPM2.5) on the expression of long non-coding RNAs (lncRNAs) in order to find new therapeutic targets for treatment of chronic obstructive pulmonary disease (COPD). HBECs were exposed to TAPM2.5 and WSPM2.5 at a series of concentrations. The microarray analysis was used to detect the lncRNA and mRNA expression profiles. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis and gene ontology (GO) enrichment were conducted to analyze the differentially expressed lncRNAs and mRNAs. Quantitative real-time PCR (qRT-PCR) was performed to confirm the differential expression of lncRNAs. Western blot was performed to study the expression of autophagy and apoptosis-associated proteins. Flow cytometry was used to detect the apoptotic cells. The results indicated that fine particulate matter (PM2.5)-induced cell damage of HBECs occurred in a dose-dependent manner. The microarray analysis indicated that treatment with TAPM2.5 and WSPM2.5 led to the alteration of lncRNA and mRNA expression profiles. LncRNA maternally expressed gene 3 (MEG3) was significantly up-regulated in HBECs after PM2.5 treatment. The results of Western blot showed that PM2.5 induced cell apoptosis and autophagy by up-regulating apoptosis-associated gene, caspase-3, and down-regulating autophagy-associated markers, Bcl-2 and LC3 expression. In addition, we demonstrated that TAPM2.5 and WSPM2.5 accelerated apoptosis of human bronchial (HBE) cells, silencing of MEG3 suppressed apoptosis and autophagy of HBE cells. These findings suggested that the lncRNA MEG3 mediates PM2.5-induced cell apoptosis and autophagy, and probably through regulating the expression of p53.

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