The Clock-partner aryl hydrocarbon receptor nuclear translocator-like, both of which play important roles in neuronal function. These studies, like most with miRs, were conducted after transient overexpression of miR-142. The goal of the present study was to identify neuronal genes affected by chronic miR-142 upregulation and that may contribute to the neuronal pathology in HAND. We report that chronic overexpression of miR-142 in a neuronal cell line leads to downregulation of expression and activity of the neurotransmittermetabolizing enzyme monoamine oxidase type A. Decrease in MAOA protein level was also confirmed in primary human AbMole Amikacin hydrate neurons that were transduced with miR-142. The MAOA 39UTR does not have any binding sites for either miR-142-3p or 5p. Previously we identified SIRT1 as a direct target of miR-142; SIRT1 is downregulated in cell lines and neurons overexpressing miR-142 and is known to induce MAOA expression. Therefore, we postulate that miR-142 decreases MAOA expression by reducing SIRT1 protein level. Accordingly, overexpression of SIRT1 restored MAOA protein expression levels. Downregulation of SIRT1 by miR-142 therefore leads to the reduction in MAOA expression and activity, and may contribute to the changes in catecholaminergic neurotransmission in HAND. In this study we have elucidated a novel molecular mechanism of miR-mediated regulation of MAOA expression neuronal cells. Chronic overexpression of miR-142 led to decrease in MAOA mRNA and protein levels, as well as a reduction in the enzyme activity. This regulation of MAOA expression and activity by miR-142 is mediated indirectly through repression of the direct miR-142-5p target, SIRT1, that otherwise 
induces MAOA expression. Decrease in MAOA expression and activity may contribute to the reported changes in neurotransmitter metabolism in HAND, ultimately leading to neuronal dysfunction. However, in brain sections from rhesus macaques with SIVE, co-localization studies with cell type markers showed that in addition to myeloid cells, miR-142 is expressed both in neurons as well. Upregulation of neuronal miR-142 expression was also reported following peripheral nerve crush and cocaine AbMole 3,4,5-Trimethoxyphenylacetic acid treatment. In order to investigate the downstream effects of such increase in neuronal miR-142 expression we compared gene expression of stable BEM17 clones expressing miR-142 to clones that were transduced with miR-null. Among the significantly differentially expressed genes, we chose to focus on MAOA for further studies. Congruent with its prime role in neurotransmitter catabolism, pharmacological and genetic evidence has linked MAOA with mood and emotion. We found that miR-142 overexpression in neuronal cell lines and neurons results in lower MAOA mRNA and protein levels, as well as enzyme activity.