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Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
MicroRNA-1228(*) inhibit apoptosis in A549 cells exposed to fine particulate matter
Xiaobo Li1, Zhen Ding2, Chengcheng Zhang1
1Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University, Dingjiaqiao 87, Nanjing, 210009, China.
Abstract:
Studies have reported associations between fine particulate matter (PM2.5) and respiratory disorders; however, the underlying mechanism is not completely clear owing to the complex components of PM2.5. microRNAs (miRNAs) demonstrate tremendous regulation to target genes, which are sensitive to exogenous stimulation, and facilitate the integrative understood of biological responses. Here, significantly modulated miRNA were profiled by miRNA microarray, coupled with bioinformatic analysis; the potential biological function of modulated miRNA were predicted and subsequently validated by cell-based assays. Downregulation of miR-1228-5p (miR-1228(*)) expression in human A549 cells were associated with PM2.5-induced cellular apoptosis through a mitochondria-dependent pathway. Further, overexpression of miR-1228(*) rescued the cellular damages induced by PM2.5. Thus, our results demonstrate that PM2.5-induced A549 apoptosis is initiated by mitochondrial dysfunction and miR-1228(*) could protect A549 cells against apoptosis. The involved pathways and target genes might be used for future mechanistic studies.
Insights
Fine particulate matter (PM2.5) exposure triggers cell death in lung cells via mitochondrial damage. However, miR-1228(*) microRNA protects these cells from PM2.5-induced apoptosis.
Area of Science:
- Environmental Health
- Molecular Biology
- Cellular Biology
Background:
- Exposure to fine particulate matter (PM2.5) is linked to respiratory diseases, but the exact mechanisms remain unclear due to PM2.5's complex composition.
- MicroRNAs (miRNAs) are crucial regulators of gene expression, sensitive to environmental factors, and offer insights into biological responses.
Purpose of the Study:
- To investigate the role of microRNAs in the cellular response to PM2.5 exposure.
- To elucidate the mechanism of PM2.5-induced apoptosis in human lung cells (A549) and identify protective miRNAs.
Main Methods:
- MicroRNA microarray profiling to identify significantly modulated miRNAs in response to PM2.5.
- Bioinformatic analysis to predict the biological functions of identified miRNAs.
- Cell-based assays to validate the function of miR-1228-5p (miR-1228(*)) in PM2.5-induced apoptosis.
Main Results:
- PM2.5 exposure led to the downregulation of miR-1228(*) expression in A549 cells.
- The downregulation of miR-1228(*) was associated with PM2.5-induced apoptosis via a mitochondria-dependent pathway.
- Overexpression of miR-1228(*) protected A549 cells from PM2.5-induced cellular damage.
Conclusions:
- PM2.5 induces apoptosis in A549 cells, initiated by mitochondrial dysfunction.
- miR-1228(*) plays a protective role against PM2.5-induced apoptosis in lung cells.
- The identified pathways and target genes provide a basis for future mechanistic studies on PM2.5 toxicity.
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