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Exp Neurobiol 2015; 24(2): 117-125
Published online June 30, 2015
https://doi.org/10.5607/en.2015.24.2.117
© The Korean Society for Brain and Neural Sciences
Juhyun Song1, Yumi Oh1,2 and Jong Eun Lee1,2*
1Department of Anatomy, 2BK21 Plus Project for Medical Sciences, and Brain Research Institute, Yonsei University College of Medicine, Seoul 120-752, Korea
Correspondence to: *To whom correspondence should be addressed.
TEL: 82-2-2228-1646, 1659, FAX: 82-2-365-0700
e-mail: jelee@yuhs.ac
Microglia regulate the secretion of various immunomediators in central nervous system diseases. Microglial autophagy is the crucial process for cell's survival and cytokine productions. Recent studies have reported that several microRNAs are involved in the autophagy system. miR-Let7A is such a microRNA that plays a role in various inflammation responses, and is magnified as a key modulator particularly in the autophagy system. In present study, we investigated whether miR-Let7A is involved in autophagy in activating microglia. Overexpression of miR-Let7A in LPS-stimulated BV2 microglial cells promoted the induction of the autophagy related factors such as LC3II, Beclin1, and ATG3. Our results suggest a potential role of miR-Let7A in the autophagy process of microglia during CNS inflammation.
Keywords: microRNA-Let7A (miR-Let7A), Microglia, Autophagy, Beclin 1, Microtubule-associated protein light chain 3 (LC3) II, ATG 3