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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Authors: | Imane Sabaouni Ahmed Moussa Brigitte Vannier Oussama Semlali Terri A Pietka Nada A Abumrad Azeddine Ibrahimi |
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Institution: | 1.Medical Biotechnology Lab (MedBiotech), Rabat Medical & Pharmacy School, Mohammed Vth Souissi University, Rabat, Morocco;2.LabTIC Laboratory, ENSA, Abdelmalek Essaadi University, Tangier, Morocco;3.Receptors, Regulation and Tumor Cells (2RTC) Laboratory, University of Poitiers, France;4.Division of Biology and Biomedical Sciences, Washington University, USA |
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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. |
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Keywords: | CD36 Fatty Acid Microarrays Metabolism angiogenesis/apoptosis Protein interaction Gene expression |
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