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Deregulation of microRNAs by HIV-1 Vpr protein leads to the development of neurocognitive disorders [differentiated SH-5Y cells]

ABSTRACT: Studies have shown that HIV-infected patients develop neurocognitive disorders characterized by neuronal dysfunction. The lack of productive infection of neurons by HIV suggests that viral and cellular proteins, with neurotoxic activities, released from HIV-1-infected target cells can cause this neuronal deregulation. The viral protein R (Vpr), a protein encoded by HIV-1, has been shown to alter the expression of various important cytokines and inflammatory proteins in infected and uninfected cells; however the mechanisms involved remain unclear. Using a human neuronal cell line, we found that Vpr can be taken up by neurons causing: (i) deregulation of calcium homeostasis, (ii) endoplasmic reticulum-calcium release, (iii) activation of the oxidative stress pathway, (iv) mitochondrial dysfunction and v- synaptic retraction. In search for the cellular factors involved, we performed microRNAs and gene array assays using human neurons (primary cultures or cell line, SH-SY5Y) that we treated with recombinant Vpr proteins. Interestingly, Vpr deregulates the levels of several microRNAs (e.g. miR-34a) and their target genes (e.g. CREB), which could lead to neuronal dysfunctions. Therefore, we conclude that Vpr plays a major role in neuronal dysfunction through deregulating microRNAs and their target genes, a phenomenon that could lead to the development of neurocognitive disorders. Human neurons SH-SY5Y were chosen to examine the impact of HIV-1 Vpr protein on gene expression

ORGANISM(S): Homo sapiens  

SUBMITTER: S A Azizi   Bassel E Sawaya  E Cohen  R Mukerjee  L Del Valle  E Brailoiu  C Power  A Bagashev  R B Lyde  M M Gayed  B B Gelman  J R Chang  B J Hawkins  B E Sawaya 

PROVIDER: E-GEOD-43535 | ArrayExpress | 2013-01-17



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