Abstract
Illicit drug abuse is highly prevalent and serves as a powerful co-factor for HIV exacerbation. Epigenetic alterations in drug abuse and HIV infection determine expression of several critical genes such as vitamin D receptor (VDR), which participates in proliferation, differentiation, cell death under both physiological and pathological conditions. On that account, active vitamin D, the ligand of VDR, is used as an adjuvant therapy to control infection, slow down progression of chronic kidney diseases, and cancer chemotherapy. Interestingly, vitamin D may not be able to augment VDR expression optimally in several instances where epigenetic contributes to down regulation of VDR; however, reversal of epigenetic corruption either by demethylating agents (DACs) or histone deacetylase (HDAC) inhibitors would be able to maximize expression of VDR in these instances.
Highlights
Drug abuse is an important public health problem in the United States, affecting both the user and their families
Optimal expression of T cell vitamin D receptor (VDR) expression was achieved with the use of Vit D and a DAC together. These investigators showed that down regulation of VDR was associated with elevated renin and Angiotensin II levels; inhibition of VDR methylation restored the VDR expression and provided the protection against HIV-induced T cell apoptosis (Chandel et al, 2013a)
Cadet and Jayanthi (2013) provides direct evidence for epigenetic regulation of transcriptional effects of chronic MA exposure on glutamate receptors, which describes the potential roles of REST, CoREST, methyl-CpG binding protein 2 (MeCP2), HDAC1, and HDAC2 in mediating MA-induced down regulation of GluA1, GluA2, and GluN1 transcription levels
Summary
PC (2015) Vitamin D receptor and epigenetics in HIV infection and drug abuse. Illicit drug abuse is highly prevalent and serves as a powerful co-factor for HIV exacerbation. Epigenetic alterations in drug abuse and HIV infection determine expression of several critical genes such as vitamin D receptor (VDR), which participates in proliferation, differentiation, cell death under both physiological and pathological conditions. Active vitamin D, the ligand of VDR, is used as an adjuvant therapy to control infection, slow down progression of chronic kidney diseases, and cancer chemotherapy. Vitamin D may not be able to augment VDR expression optimally in several instances where epigenetic contributes to down regulation of VDR; reversal of epigenetic corruption either by demethylating agents (DACs) or histone deacetylase (HDAC) inhibitors would be able to maximize expression of VDR in these instances
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