Role of microRNA-4516 involved autophagy associated with exposure to fine particulate matter
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Xiaobo Li1, Yang Lv2, Jihong Hao3, Hao Sun1, Na Gao1, Chengcheng Zhang1, Runze Lu1, Shizhi Wang1, Lihong Yin1, Yuepu Pu1, Rui Chen1,4
1Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University, Nanjing 210009, China
2Department of Histology and Embryology, Hebei North University, Zhangjiakou 075000, China
3Clinical Laboratory of The Second Hospital, Hebei Medical University, Shijiazhuang 050000, China
4State Key Laboratory of Bioelectronics, Southeast University, Nanjing 210096, China
Rui Chen, email: email@example.com
Keywords: PM2.5, metal, autophagy, ribosome, microRNA
Received: February 19, 2016 Accepted: May 23, 2016 Published: June 13, 2016
Metals are vital toxic components of fine particulate matter (PM2.5). Cellular responses to exposure to PM2.5 or PM metal components remain unknown. Post-transcriptional profiling and subsequent cell- and individual-based assays implied that the metal ion-binding miR-4516/RPL37/autophagy pathway could play a critical role in cellular responses to PM2.5 and PM metal stresses. miR-4516 was up-regulated in A549 cells exposed to PM2.5 and in the serum of individuals living in a city with moderate air pollution. The expression levels of the miR-4516 target genes, namely, RPL37 and UBA52, were involved in ribosome function and inhibited by exposure to PM2.5 and PM metal components. Autophagy in A549 cells was induced by PM2.5 exposure as a response to decreased RPL37 expression. Moreover, enhanced miR-4516 expression was positively correlated with the augmentation of the internal burden of aluminum and lead in individuals living in a city with moderate air pollution. Hereby, the miR-4516/RPL37/autophagy pathway may represent a novel mechanism that mediates responses to PM metal components.
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