Gene expression profiling reveals key genes and pathways related to the development of non-alcoholic fatty liver disease



Título del documento: Gene expression profiling reveals key genes and pathways related to the development of non-alcoholic fatty liver disease
Revue: Annals of hepatology
Base de datos: PERIÓDICA
Número de sistema: 000409077
ISSN: 1665-2681
Autores: 1
2
1
Instituciones: 1Harbin Medical University, Fourth Affiliated Hospital, Harbin, Heilongjiang. China
2Harbin Medical University, First Affiliated Hospital, Harbin, Heilongjiang. China
Año:
Volumen: 15
Número: 2
Paginación: 190-199
País: México
Idioma: Inglés
Tipo de documento: Artículo
Enfoque: Aplicado, descriptivo
Resumen en inglés This study aims to identify key genes and pathways involved in non-alcoholic fatty liver disease (NAFLD). The dataset GSE48452 was downloaded from Gene Expression Omnibus, including 14 control liver samples, 27 healthy obese samples, 14 steatosis samples and 18 nonalcoholic steatohepatitis (NASH) samples. Differentially expressed genes (DEGs) between controls and other samples were screened through LIMMA package. Then pathway enrichment analysis for DEGs was performed by using DAVID, and alterations of enriched pathways were determined. Furthermore, protein-protein interaction (PPI) networks were constructed based on the PPI information from HPRD database, and then, networks were visualized through Cytoscape. Additionally, interactions between microRNAs (miRNAs) and pathways were analyzed via Fisher’s exact test. Results. A total of 505, 814 and 783 DEGs were identified for healthy obese, steatosis and NASH samples in comparison with controls, respectively. DEGs were enriched in ribosome (RPL36A, RPL14, etc.), ubiquitin mediated proteolysis (UBE2A, UBA7, etc.), focal adhesion (PRKCA, EGFR, CDC42, VEGFA, etc.), FcγR-mediated phagocytosis (PRKCA, CDC42, etc.), and so on. The 27 enriched pathways gradually deviated from baseline (namely, controls) along with the changes of obese-steatosis-NASH. In PPI networks, PRKCA interacted with EGFR and CDC42. Besides, hsa-miR-330-3p and hsa-miR-126 modulated focal adhesion through targeting VEGFA and CDC42. Conclusions. Conclusions. The Conclusions. identified DEGs (PRKCA, EGFR, CDC42, VEGFA), disturbed pathways (ribosome, ubiquitin mediated proteolysis, focal adhesion, FcγR-mediated phagocytosis, etc.) and miRNAs (hsa-miR-330-3p, hsa-miR-126, etc.) might be closely related to NAFLD progression. These results might contribute to understanding NAFLD mechanism, conducting experimental researches, and designing clinical practices
Disciplinas: Medicina
Palabras clave: Gastroenterología,
Genética,
Hígado graso no alcohólico,
Esteatohepatitis,
Patogénesis,
Expresión génica
Keyword: Medicine,
Gastroenterology,
Genetics,
Non alcoholic fatty liver,
Steatohepatitis,
Pathogenesis,
Gene expression
Texte intégral: Texto completo (Ver PDF)