title: Microarray Study of Pathway Analysis Expression Profile Associated with MicroRNA-29a with Regard to Murine Cholestatic Liver Injuries.
abstract: Accumulating evidence demonstrates that microRNA-29 (miR-29) expression is prominently decreased in patients with hepatic fibrosis, which consequently stimulates hepatic stellate cells' (HSCs) activation. We used a cDNA microarray study to gain a more comprehensive understanding of genome-wide gene expressions by adjusting miR-29a expression in a bile duct-ligation (BDL) animal model.
  
  
  METHODS
  Using miR-29a transgenic mice and wild-type littermates and applying the BDL mouse model, we characterized the function of miR-29a with regard to cholestatic liver fibrosis. Pathway enrichment analysis and/or specific validation were performed for differentially expressed genes found within the comparisons.
  
  
  RESULTS
  Analysis of the microarray data identified a number of differentially expressed genes due to the miR-29a transgene, BDL, or both. Additional pathway enrichment analysis revealed that TGF-β signaling had a significantly differential activated pathway depending on the occurrence of miR-29a overexpression or the lack thereof. Furthermore, overexpression was found to elicit changes in Wnt/β-catenin after BDL.
  
  
  CONCLUSIONS
  This study verified that an elevated miR-29a level could alleviate liver fibrosis caused by cholestasis. Furthermore, the protective effects of miR-29a correlate with the downregulation of TGF-β and associated with Wnt/β-catenin signal pathway following BDL.
authors.affiliation: Genomics and Proteomics Core Laboratory, Department of Medical Research, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, 833 Kaohsiung, Taiwan. raymond.pinus@gmail.com.
authors.forename: Sung-Chou
authors.initials: SC
authors.lastname: Li
authors.affiliation: Genomics and Proteomics Core Laboratory, Department of Medical Research, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, 833 Kaohsiung, Taiwan. wangfs@ms33.hinet.net.
authors.forename: Feng-Sheng
authors.initials: FS
authors.lastname: Wang
authors.affiliation: Department of Anesthesiology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, 833 Kaohsiung, Taiwan. yaling453@yahoo.com.tw.
authors.forename: Ya-Ling
authors.initials: YL
authors.lastname: Yang
authors.affiliation: Department of Pediatrics, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, 833 Kaohsiung, Taiwan. tmm@cgmh.org.tw.
authors.forename: Mao-Meng
authors.initials: MM
authors.lastname: Tiao
authors.affiliation: Department of Surgery, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, 833 Kaohsiung, Taiwan. jhchuang@cgmh.org.tw.
authors.forename: Jiin-Haur
authors.initials: JH
authors.lastname: Chuang
authors.affiliation: Department of Pediatrics, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, 833 Kaohsiung, Taiwan. yhhuang123@yahoo.com.tw.
authors.forename: Ying-Hsien
authors.initials: YH
authors.lastname: Huang
mesh_terms: D000818:Animals; D002779:Cholestasis / Q000150:complications* / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D036341:Intercellular Signaling Peptides and Proteins / Q000032:analysis / Q000378:metabolism; D008099:Liver / Q000378:metabolism / Q000473:pathology*; D008103:Liver Cirrhosis / Q000150:complications* / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D035683:MicroRNAs / Q000235:genetics*; D015398:Signal Transduction; D059467:Transcriptome; D016212:Transforming Growth Factor beta / Q000032:analysis / Q000378:metabolism; D015854:Up-Regulation; D060449:Wnt Signaling Pathway
chemical_list: C501127:Dkk1 protein, mouse; D036341:Intercellular Signaling Peptides and Proteins; C547014:MIRN29 microRNA, mouse; D035683:MicroRNAs; D016212:Transforming Growth Factor beta
keywords: TGF-β signaling pathway; Wnt signaling pathway; bile duct ligation; cholestasis; liver fibrosis; miR-29a