HIV-1 gp120 Upregulates Brain-Derived Neurotrophic Factor (BDNF) Expression in BV2 Cells via the Wnt/β-Catenin Signaling Pathway

Yongdi Wang, Jinxu Liao, Shao-Jun Tang, Jianhong Shu, Wenping Zhang

Research output: Contribution to journalArticle

7 Scopus citations


HIV-1 gp120 plays a critical role in the pathogenesis of HIV-associated pain, but the underlying molecular mechanisms are incompletely understood. This study aims to determine the effect and possible mechanism of HIV-1 gp120 on BDNF expression in BV2 cells (a murine-derived microglial cell line). We observed that gp120 (10 ng/ml) activated BV2 cells in cultures and upregulated proBDNF/mBDNF. Furthermore, gp120-treated BV2 also accumulated Wnt3a and β-catenin, suggesting the activation of the Wnt/β-catenin pathway. We demonstrated that activation of the pathway by Wnt3a upregulated BDNF expression. In contrast, inhibition of the Wnt/β-catenin pathway by either DKK1 or IWR-1 attenuated BDNF upregulation induced by gp120 or Wnt3a. These findings collectively suggest that gp120 stimulates BDNF expression in BV2 cells via the Wnt/β-catenin signaling pathway.

Original languageEnglish (US)
Pages (from-to)199-208
Number of pages10
JournalJournal of Molecular Neuroscience
Issue number2
StatePublished - Jun 1 2017



  • BDNF
  • HIV-1 gp120
  • Microglia
  • Wnt/β-catenin signaling

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience

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