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.
Highlights
CD36 gene encodes a membrane glycoprotein, and has been identified in wide variety cells types, including platelets, monocytes, and erythroblast, capillary endothelial and mammary epithelial cells [1,2,3,4,5,6]
CD36 is a membrane glycoprotein highly expressed in heart tissue
Two sets of studies were done to identify a comprehensive set of genes that are differentially regulated by CD36 expression in the heart
Summary
CD36 gene encodes a membrane glycoprotein, and has been identified in wide variety cells types, including platelets, monocytes, and erythroblast, capillary endothelial and mammary epithelial cells [1,2,3,4,5,6]. CD36 ( known as platelet glycoprotein IV or IIIb) is a membrane glycoprotein highly expressed in heart tissue. It was shown that CD36 works as receptor/transporter of long chain fatty acids (FA) in muscle tissue and is proposed as one of thrombospondine receptor in endothelial cells [5]. In 2002 and 2007, we used respectively the Affymetrix and the Agilent technologies to analyze CD36 involvement in the fatty acids uptake and heart hypertrophy [7, 3,4,5, 8]. We propose to compare results obtained from the two microarrays technologies and investigate the consequences of CD36 absence
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