HIV associated dementia and HIV encephalitis II: Genes on chromosome 22 expressed in individually microdissected Globus pallidus neurons (Preliminary analysis)

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Title	*HIV associated dementia and HIV encephalitis II: Genes on chromosome 22 expressed in individually microdissected Globus pallidus* neurons (Preliminary analysis)**
Authors	Paul Shapshak^{1, 2}*, Robert Duncan³, Pandajarasamme Kangueane^{4, 5}, Charurut Somboonwit^{1, 6}, John Sinnott^{1, 6}, Deborah Commins^{7, 8}, Elyse Singer^{8, 9}, Andrew Levine^{8, 9}
Affiliation	¹Division of Infectious Disease and International Medicine, Tampa General Hospital, USF Health, Tampa, FL 33601; ²Department of Psychiatry & Behavioral Medicine, University of South Florida, College of Medicine, Tampa, FL 33613; ³Department of Epidemiology, University of Miami Miller School of Medicine, Miami, FL 33136; ⁴Biomedical Informatics, Pondicherry 607 402, India; ⁵AIMST University, Malaysia 08100; ⁶Clinical Research Unit, Hillsborough Health Department, Tampa, FL 33602; ⁷Department of Pathology, USC School of Medicine, Los Angeles, CA 90089; ⁸National Neurological AIDS Bank, UCLA School of Medicine, Westwood, CA 90095; ⁹Department of Neurology, UCLA School of Medicine, Westwood, CA 90095
Email	pshapshak@gmail.com; *Corresponding author
Phone	843-754-0702
Fax	813-844-8013
Article Type	Hypothesis
Date	Received May 10, 2011; Accepted May 13, 2011; Published May 26, 2011
Abstract	We analyzed RNA gene expression in neurons from 16 cases in four categories, HIV associated dementia with HIV encephalitis (HAD/HIVE), HAD alone, HIVE alone, and HIV-1-positive (HIV+)with neither HAD nor HIVE. We produced the neurons by laser capture microdissection (LCM) from cryopreserved Globus pallidus. Of 55,000 gene fragments analyzed, expression of 197 genes was identified with significance (p = 0.005).We examined each gene for its position in the human genome and found a non-stochastic occurrence for only seven genes, on chromosome 22. Six of the seven genes were identified, CSNK1E (casein kinase 1 epsilon), DGCR8 (Di George syndrome critical region 8), GGA1 (Golgi associated gamma adaptin ear containing ARF binding protein 1), MAPK11 (mitogen activated protein kinase 11), SMCR7L (Smith-Magenis syndrome chromosome region candidate 7-like), andTBC1D22A (TBC1 domain family member 22A). Six genes (CSNK1E, DGCR8, GGA1, MAPK11, SMCR7L, and one unidentified gene) had similar expression profiles across HAD/HIVE, HAD, and HIVE vs. HIV+ whereas one gene (TBC1D22A) had a differing gene expression profile across these patient categories. There are several mental disease-related genes including miRNAs on chromosome 22 and two of the genes (DGCR8 and SMCR7L) identified here are mental disease-related. We speculate that dysregulation of gene expression may occur through mechanisms involving chromatin damage and remodeling. We conclude that the pathogenesis of NeuroAIDS involves dysregulation of expression of mental disease-related genes on chromosome 22 as well as additional genes on other chromosomes. The involvement of these genes as well as miRNA requires additional investigation since numerous genes appear to be involved.
Keywords	Chromosome 22, gene expression, network, pathway, miRNA, HAD, HIVE, LCM, Globus pallidus, neuron, brain.
Citation	Shapshak et al. Bioinformation 6(5): 183-186 (2011)
Edited by	Peter N Pushparaj
ISSN	0973-2063
Publisher	Biomedical Informatics
License	This is an Open Access article which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. This is distributed under the terms of the Creative Commons Attribution License.