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  • Original Article
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Novel genes and cellular pathways related to infection with adenovirus-36 as an obesity agent in human mesenchymal stem cells

Abstract

Objective:

The objective of this study was to investigate the molecular mechanisms underlying adenovirus-36 (Ad-36)-induced obesity by the identification of novel genes and cellular pathways.

Design:

Viral growth, intracellular lipid accumulation and gene expression profiles were determined in human mesenchymal stem cells (hMSCs) infected with Ad-36 or Ad-2. A microarray assay and gene set enrichment analysis (GSEA) were performed to assess alterations in global gene expression profiles.

Results:

Ad-36, but not Ad-2, induced lipid accumulation and upregulated adipogenesis-related genes. There was no difference in viral growth between Ad-36 infection and Ad-2 infection in hMSCs. GSEA revealed that Ad-36 infection was more frequently associated with activation of novel pathways, including the PPAR-gamma signaling pathway, and inflammation compared with Ad-2 infection, raising the possibility that these pathways may be key regulators of Ad-36-induced adipogenesis.

Conclusion:

This study may help foster a better understanding of the roles of several cellular factors in Ad-36-induced obesity.

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Acknowledgements

This study was supported by a grant from the GRRC of the Catholic University of Korea, the Biogreen21 Program (PJ007186) of Rural Development of Administration, MKE and KOTEF through the Human Resource Training Project for Strategic Technology, and Medical Research Center (2010-0029474) programs funded by the Ministry of Science and Technology, Republic of Korea. H-N Na was supported by Hi Seoul Science (Humanities) Fellowship funded by the Seoul Scholarship Foundation.

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Correspondence to J-H Nam.

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Supplementary Information accompanies the paper on International Journal of Obesity website

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Na, HN., Kim, H. & Nam, JH. Novel genes and cellular pathways related to infection with adenovirus-36 as an obesity agent in human mesenchymal stem cells. Int J Obes 36, 195–200 (2012). https://doi.org/10.1038/ijo.2011.89

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