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Long noncoding RNA MIAT2 alleviates lipopolysaccharide‐induced inflammatory damage in WI‐38 cells by sponging microRNA‐15
Author(s) -
Zhang Hong,
Zhao Jing,
Shao Peng
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29263
Subject(s) - viability assay , apoptosis , lipopolysaccharide , western blot , microrna , microbiology and biotechnology , inflammation , cell , biology , reverse transcription polymerase chain reaction , chemistry , immunology , messenger rna , gene , biochemistry
Neonatal pneumonia is a high neonatal mortality disease. We studied the function and mechanism of long noncoding RNA myocardial infarction‐associated transcript 2 (lncRNA MIAT2) on lipopolysaccharide (LPS)‐induced inflammation in WI‐38 cells. Cell Counting Kit‐8 and apoptosis assay were respectively used to detect the functions of LPS, MIAT2, and microRNA‐15 (miR‐15) on viability and apoptosis. MIAT2 and miR‐15 expressions were changed by cell transfection. Moreover, reverse transcription‐quantitative polymerase chain reaction (RT‐qPCR), western blot, and enzyme‐linked immunosorbent assay were used to detect the expressions of interleukin (IL)‐6 and monocyte chemoattractant protein‐1 (MCP‐1). The levels of Bax, cleaved‐caspase‐3, and cell pathways‐related proteins were tested by western blot. Besides, the levels of miR‐15 and MIAT2 were tested by RT‐qPCR. We found that LPS declined cell viability and heightened apoptosis and levels of Bax, cleaved‐caspase‐3, IL‐6, and MCP‐1. MIAT2 was negatively regulated by LPS and it alleviated LPS‐induced damage. Furthermore, MIAT2 reversely regulated miR‐15 and miR‐15 mimic could reverse the effects of MIAT2. Finally, MIAT2 restrained the p38MAPK and NF‐κB pathways by downregulating miR‐15. In conclusion, MIAT2 alleviated LPS‐induced inflammation damage in WI‐38 cells by sponging miR‐15 via p38MAPK and NF‐κB pathways.