Role of microRNA-4516 involved autophagy associated with exposure to fine particulate matter

Abstract

// Xiaobo Li 1 , Yang Lv 2 , Jihong Hao 3 , Hao Sun 1 , Na Gao 1 , Chengcheng Zhang 1 , Runze Lu 1 , Shizhi Wang 1 , Lihong Yin 1 , Yuepu Pu 1 , Rui Chen 1, 4 1 Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University, Nanjing 210009, China 2 Department of Histology and Embryology, Hebei North University, Zhangjiakou 075000, China 3 Clinical Laboratory of The Second Hospital, Hebei Medical University, Shijiazhuang 050000, China 4 State Key Laboratory of Bioelectronics, Southeast University, Nanjing 210096, China Correspondence to: Rui Chen, email: 101011816@seu.edu.cn Keywords: PM 2.5 , metal, autophagy, ribosome, microRNA Received: February 19, 2016      Accepted: May 23, 2016      Published: June 13, 2016 ABSTRACT Metals are vital toxic components of fine particulate matter (PM 2.5 ). Cellular responses to exposure to PM 2.5 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 PM 2.5 and PM metal stresses. miR-4516 was up-regulated in A549 cells exposed to PM 2.5 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 PM 2.5 and PM metal components. Autophagy in A549 cells was induced by PM 2.5 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.