H-N Na1, H Kim, J-H Nam. 1. Department of Biotechnology, The Catholic University of Korea, Bucheon, Korea.
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.
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.
Authors: P K Berger; N K Pollock; E M Laing; S J Warden; K M Hill Gallant; D B Hausman; R A Tripp; L D McCabe; G P McCabe; C M Weaver; M Peacock; R D Lewis Journal: J Clin Endocrinol Metab Date: 2014-06-13 Impact factor: 5.958
Authors: Jorge Barrera-Alcocer; Leonel García-Benavides; José F Muñoz-Valle; Ulises de la Cruz-Mosso; Ramón A González; Sonia Luquín; Luz Del C Alarcón-Romero; Linda A Marino-Ortega; Ines Matia-Garcia; Isela Parra-Rojas Journal: Diabetes Metab Syndr Obes Date: 2021-02-03 Impact factor: 3.168