The Whole Genome Expression Analysis using Two Microarray Technologies to Identify Gene Networks That Mediate the Myocardial Phenotype of CD36 Deficiency

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Title	The Whole Genome Expression Analysis using Two Microarray Technologies to Identify Gene Networks That Mediate the Myocardial Phenotype of CD36 Deficiency
Authors	Imane Sabaouni¹, Ahmed Moussa²*, Brigitte Vannier³, Oussama Semlali¹, Terri A Pietka⁴, Nada A Abumrad⁴ & Azeddine Ibrahimi¹
Affiliation	¹Medical Biotechnology Lab (MedBiotech), Rabat Medical & Pharmacy School, Mohammed Vth Souissi University, Rabat, Morocco; ²LabTIC Laboratory, ENSA, Abdelmalek Essaadi University, Tangier, Morocco; ³Receptors, Regulation and Tumor Cells (2RTC) Laboratory, University of Poitiers, France; ⁴Division of Biology and Biomedical Sciences, Washington University, USA
Email	amoussa@uae.ac.ma; *Corresponding author
Article Type	Hypothesis
Date	Received January 27, 2013; Accepted September 30, 2013; Published October 16, 2013
Abstract	We have previously shown that CD36 is a membrane protein that facilitates long chain fatty acid (FA) transport by muscle tissues. We also documented the significant impact of muscle CD36 expression on heart function, skeletal muscle insulin sensitivity as well as on overall metabolism. To identify a comprehensive set of genes that are differentially regulated by CD36 expression in the heart, we used two microarray technologies (Affymetrix and Agilent) to compare gene expression in heart tissues from CD36 KnocK-Out (KO-CD36) versus wild type (WT-CD36) mice. The obtained results using the two technologies were similar with around 35 genes differentially expressed using both technologies. Absence of CD36 led to down-regulation of the expression of three groups of genes involved in pathways of FA metabolism, angiogenesis/apoptosis and structure. These data are consistent with the fact that the CD36 protein binds FA and thrombospondin 1 invoved respectively in lipid metabolism and anti-angiogenic activities. In conclusion, our findings led to validate our data analysis workflow and identify specific pathways, possibly underlying the phenotypic abnormalities in CD36 Knock -Out hearts.
Keywords	CD36, Fatty Acid, Microarrays, Metabolism, angiogenesis/apoptosis, Protein interaction, Gene expression.
Citation	Sabaouni et al. Bioinformation 9(17): 849-852 (2013)
Edited by	P Kangueane
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.