MiR-133b-5p regulates the expression of the heat shock protein 70 during rat neuronal cell apoptosis induced by the gp120 V3 loop peptide.

Abstract

Neuronal cell dysfunction and apoptosis, the main causes of HIV-associated dementia, and its underlying mechanism are important unsolved health problems. Many research reports suggest that miRNAs regulate HIV-1-induced apoptosis. We used the HIV-1 gp120 V3 Loop peptide to induce primary rat cortical neurons apoptosis. Next, we used a microRNA microarray to identify the significant changes of miRNA in the rat cortical neurons treated with the gp120 V3 loop peptide. We used western blot and real-time PCR to measure the regulation of heat shock protein 70 by rno-miR-133b-5p. In response to the gp120 V3 loop peptide treatment, rat cortical neurons exhibited 11 up-regulated and 21 down-regulated miRNAs. We further examined miR-133b-5p, a microRNA that was up-regulated more than 118-fold. In addition, both HSP70 mRNA and protein expression were dose-dependent in rats cortical neurons treated with gp120 V3 loop peptide for 48 hr. MiR-133b-5p could regulate heat shock protein 70 (HSP70) at both transcription and translation levels. Rno-miR-133b-5p might be less significant for the gp120 V3 loop peptide induced neuron apoptosis. Thus, we discovered a potential new target for the regulation of HIV-1 gp120- induced apoptosis.