Journal
NANOTOXICOLOGY
Volume 14, Issue 5, Pages 638-653Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/17435390.2020.1731857
Keywords
LncRNA PEAMIR; miR-29b-3p; ceRNA; PM2; 5 exposure; I; R injury
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Funding
- National Natural Science Foundation of China [81704110, 81700243]
- subject of Jiangsu Province Hospital of Chinese Medicine [y2018rc36, Y17020, Y2017CX13]
- Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)
- Open Projects of the Discipline of Chinese Medicine of Nanjing University of Chinese Medicine - Subject of Academic priority discipline of Jiangsu Higher Education Institutions [ZYX03KF039]
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The sensitivity of myocardium is enhanced to ischemia/reperfusion (I/R) injury under PM2.5 exposure. It is still under prelude for lncRNA-miRNA pair in the study of aggravated myocardial I/R injury under PM2.5 exposure. In this study, we first built a rat model of 30 min ischemia and 24 h reperfusion followed PM2.5 (6.0 mg/kg) exposure. We found PM2.5 exposure could obviously aggravate I/R injury in the fields of myocardium damage, apoptosis levels and cardiac function which were evaluated by TTC staining, TUNEL and echocardiography, respectively. Then, based on results of sequencing and RT-qPCR, we selected NONRATT003473.2 in the follow-up experiments and named this lncRNA as PM2.5 exposure aggravated myocardial I/R injury lncRNA (PEAMIR). Consistent with the results rat model, we confirmed PEAMIR to be a protective lncRNA against PM + HR triggered damages in H9c2 cells. Next, according to the bioinformatics analysis from miRanda database and a series of gain- and loss-of-function experiments, we proved PEAMIR to be a ceRNA for miR-29b-3p to inhibit cardiac inflammation and apoptosis. Finally, using Target-Scan database, the conserved binding sites for miR-29b-3p was identified in the 3'UTR of PI3K (p85a), a key protein of apoptosis. Our subsequent experiments validated the regulatory relationship between PEAMIR-miR-29b-3p ceRNA pair and PI3K (p85a)/Akt/GSK3b/p53 cascade pathway. In conclusion, our study demonstrated the role and mechanism of PEAMIR in the augment of I/R injury under PM2.5 exposure, suggesting a promising strategy for the prevention and treatment of I/R injury under PM2.5 exposure.
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