Extracellular microvesicles-derived from microglia treated with unaggregated α-synuclein attenuate mitochondrial fission and toxicity-induced by Parkinsonian toxin MPP

  • Biochem Biophys Res Commun. 2019 Oct 1;517(4):642-647. doi: 10.1016/j.bbrc.2019.07.084.
Na Li  1 ,  Yufeng Wu  2 ,  Liangyi Zhu  1 ,  Yang Huang  1 ,  Zongran Liu  1 ,  Min Shi  3 ,  David Soltys  3 ,  Jing Zhang  4 ,  Qing Chang  5
Affiliations
  • 1. Department of Pathology, School of Basic Medical Sciences, Peking University Third Hospital, Peking University Health Science Center, Beijing, 100191, China.
  • 2. Department of Laboratory Medicine, Peking University Third Hospital, Peking University Health Science Center, Beijing, China.
  • 3. Department of Pathology, University of Washington, Seattle, WA, 98106, USA.
  • 4. Department of Pathology, University of Washington, Seattle, WA, 98106, USA. Electronic address: [email protected].
  • 5. Department of Pathology, School of Basic Medical Sciences, Peking University Third Hospital, Peking University Health Science Center, Beijing, 100191, China. Electronic address: [email protected].
PMID: 31402119 DOI: 10.1016/j.bbrc.2019.07.084
Abstract

Biological functions of extracellular vesicles (EVs) are being discovered to be critical in neurodegenerative disorders, including Parkinson's disease (PD). A previous study using cellular models of PD has suggested that EVs derived from microglia exposed to aggregated α-synuclein (α-Syn) leads to enhanced neurotoxicity. However, the function of EVs derived from microglia not treated with aggregated a-Syn or treated with monomeric α-Syn are unclear. Here, employing a widely used cellular model of PD, i.e. SH-SY5Y cells treated with MPP+, a well-established parkinsonian toxicant, we revealed that microglial EVs, when not stimulated by aggregated α-Syn, appeared to be protective, and the mechanisms, though remain to be defined further, appeared to involve mitochondrial dynamics, especially mitochondrial fission.

Keywords
MPP(+); Microglia-derived EVs; Mitochondrial fission/fusion; PD cell model; α-synuclein.
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