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  • ISSN 1674-8301
  • CN 32-1810/R
Volume 30 Issue 6
Oct.  2016
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Qiuzi Wu, Hongfei Xu, Wei Wang, Fei Chang, Yu Jiang, Yongjian Liu. Retrograde trafficking of VMAT2 and its role in protein stability in non-neuronal cells[J]. The Journal of Biomedical Research, 2016, 30(6): 502-509. DOI: 10.7555/JBR.30.20160061
Citation: Qiuzi Wu, Hongfei Xu, Wei Wang, Fei Chang, Yu Jiang, Yongjian Liu. Retrograde trafficking of VMAT2 and its role in protein stability in non-neuronal cells[J]. The Journal of Biomedical Research, 2016, 30(6): 502-509. DOI: 10.7555/JBR.30.20160061
shu

Retrograde trafficking of VMAT2 and its role in protein stability in non-neuronal cells

  • 1.

    Department of Physiology, School of Basic Medical Science, Nanjing Medical University, Nanjing, Jiangsu 211166, China

  • 2.

    Department of Pharmacology & Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, USA

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This work was supported by the National Nature Science Foundation of China (Grant No.31371436 and No. 8157051134) and by the laboratory start-up grant from Nanjing Medical University to Y. Liu. We also thank Dr. Steven Cheng's lab for the assistance with confocal laser microscopy. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

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  • Received Date: April 13, 2016
  • Revised Date: May 07, 2016
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    • Abstract
  • Increasing evidence suggests that the impaired neuroprotection of vesicular monoamine transporter 2 (VMAT2) contributes to the pathogenesis of Parkinson's disease. That has been linked to aberrant subcellular retrograde trafficking as strongly indicated by recent genomic studies on familial Parkinson's diseases. However, whether VMAT2 function is regulated by retrograde trafficking is unknown. By using biochemistry and cell biology approaches, we have shown that VMAT2 was stringently localized to the trans-Golgi network and underwent retrograde trafficking in non-neuronal cells. The transporter also interacted with the key component of retromer, Vps35, biochemically and subcellularly. Using specific siRNA, we further showed that Vps35 depletion altered subcellular localization of VMAT2. Moreover, siRNA-mediated Vps35 knockdown also decreased the stability of VMAT2 as demonstrated by the reduced half-life. Thus, our work suggested that altered vesicular trafficking of VMAT2 may play a vital role in neuroprotection of the transporter as well as in the pathogenesis of Parkinson's disease.
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    1. Chen Q, Sun M, Han X, et al. Structural determinants specific for retromer protein sorting nexin 5 in regulating subcellular retrograde membrane trafficking. J Biomed Res, 2023, 37(6): 492-506. DOI:10.7555/JBR.37.20230112
    2. Xu H, Chang F, Jain S, et al. SNX5 targets a monoamine transporter to the TGN for assembly into dense core vesicles by AP-3. J Cell Biol, 2022, 221(5): e202106083. DOI:10.1083/jcb.202106083
    3. Grochowska KM, Andres-Alonso M, Karpova A, et al. The needs of a synapse-How local organelles serve synaptic proteostasis. EMBO J, 2022, 41(7): e110057. DOI:10.15252/embj.2021110057
    4. Yang Z, Li Z, Teasdale RD. Retromer dependent changes in cellular homeostasis and Parkinson's disease. Essays Biochem, 2021, 65(7): 987-998. DOI:10.1042/EBC20210023
    5. Kong Y, Zhou H, Feng H, et al. Elucidating the Relationship Between Diabetes Mellitus and Parkinson's Disease Using 18F-FP-(+)-DTBZ, a Positron-Emission Tomography Probe for Vesicular Monoamine Transporter 2. Front Neurosci, 2020, 14: 682. DOI:10.3389/fnins.2020.00682
    6. Limanaqi F, Biagioni F, Gambardella S, et al. Interdependency Between Autophagy and Synaptic Vesicle Trafficking: Implications for Dopamine Release. Front Mol Neurosci, 2018, 11: 299. DOI:10.3389/fnmol.2018.00299

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