HIV-infected microglia mediate cathepsin B-induced neurotoxicity

@article{Zenn2015HIVinfectedMM,
  title={HIV-infected microglia mediate cathepsin B-induced neurotoxicity},
  author={Frances M. Zen{\'o}n and Yisel M. Cantres-Rosario and Radhika Adiga and Mariangeline Gonzalez and Eillen J. Rodriguez-Franco and Dianne Langford and Loyda M. Mel{\'e}ndez},
  journal={Journal of NeuroVirology},
  year={2015},
  volume={21},
  pages={544-558}
}
HIV-1-infected mononuclear phagocytes release soluble factors that affect the homeostasis in tissue. HIV-1 can prompt metabolic encephalopathy with the addition of neuronal dysfunction and apoptosis. Recently, we reported that HIV-1 enhances the expression and secretion of bioactive cathepsin B in monocyte-derived macrophages, ultimately contributing to neuronal apoptosis. In this research, we asked if microglia respond to HIV infection similarly by modifying the expression, secretion, and… CONTINUE READING

7 Figures & Tables

Connections & Topics

Mentioned Connections BETA
HIV - infected microglia secreted significantly greater levels of cathepsin B , cystatin B , and cystatin C compared to uninfected cells .
HIV - infected microglia secreted significantly greater levels of cathepsin B , cystatin B , and cystatin C compared to uninfected cells .
HIV - infected microglia secreted significantly greater levels of cathepsin B , cystatin B , and cystatin C compared to uninfected cells .
Increased microglia - derived cathepsin B , cystatin B , and cystatin C and caspase-3 + neurons were detected in HIVE brains compared to controls .
HIV - infected microglia secreted significantly greater levels of cathepsin B , cystatin B , and cystatin C compared to uninfected cells .
All Topics