title: Synchronized expressions of hepatic stellate cells and their transactivation and liver regeneration during liver injury in an animal model of cholestasis.
abstract: BACKGROUND
  There is much known about hepatic stellate cells (HSCs) during liver injury. However, some aspects remain unclear, such as the natural expression levels of HSCs during the days to weeks after liver injury. Does liver regeneration start the same time as the injury process?
  
  
  METHODS
  Fifty-four male Wistar rats aged 7 to 8 weeks, weighing 200 to 320 g each were subjected to bile duct ligation (BDL). After surgery, they were killed at different times post-BDL. Collagen deposition was analyzed, and immunohistochemical staining of α-smooth muscle actin (α-SMA), vimentin, matrix metalloproteinase-2 (MMP-2), tissue inhibitor matrix metalloproteinase-1, and proliferating cell nuclear antigen antibody (PCNA) was performed to evaluate HSCs and liver regeneration.
  
  
  RESULTS
  The expression of α-SMA was seen as early as day 3 post-BDL, which started from peribiliary to perisinusoidal, and was seen throughout the whole liver sections on day 28 post-BDL. Similar expression patterns were seen in MMP-2 staining. The PCNA expression was strongest around the perisinusoidal area. These expression patterns were not observed in the sham-operated rats.
  
  
  CONCLUSIONS
  The activation of HSCs showed a synchronized fibrogenic process and liver regeneration from days to weeks after liver injury. Matrix degradation was thus found to increase in accordance with chronic liver injury, which thus led to an excessive collagen deposition.
authors.affiliation: Department of Pediatric Surgery, Reproductive and Developmental Medicine, Kyushu University, Fukuoka, Japan. safira@pedsurg.med.kyushu-u.ac.jp
authors.forename: Fatima Safira
authors.initials: FS
authors.lastname: Alatas
authors.forename: Kouji
authors.initials: K
authors.lastname: Masumoto
authors.forename: Toshiharu
authors.initials: T
authors.lastname: Matsuura
authors.forename: Makoto
authors.initials: M
authors.lastname: Hayashida
authors.forename: Isamu
authors.initials: I
authors.lastname: Saeki
authors.forename: Kenichi
authors.initials: K
authors.lastname: Kohashi
authors.forename: Yoshinao
authors.initials: Y
authors.lastname: Oda
authors.forename: Tomoaki
authors.initials: T
authors.lastname: Taguchi
mesh_terms: D000199:Actins / Q000096:biosynthesis; D000818:Animals; D001652:Bile Ducts / Q000601:surgery; D002779:Cholestasis / Q000378:metabolism / Q000473:pathology*; D003094:Collagen / Q000096:biosynthesis; D004195:Disease Models, Animal; D016326:Extracellular Matrix Proteins / Q000096:biosynthesis*; D055166:Hepatic Stellate Cells / Q000378:metabolism* / Q000473:pathology; D008026:Ligation; D008115:Liver Regeneration / Q000502:physiology*; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000096:biosynthesis; D008938:Mitosis; D018809:Proliferating Cell Nuclear Antigen / Q000096:biosynthesis; D051381:Rats; D017208:Rats, Wistar; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000096:biosynthesis; D014746:Vimentin / Q000096:biosynthesis
chemical_list: D000199:Actins; D016326:Extracellular Matrix Proteins; D018809:Proliferating Cell Nuclear Antigen; D019715:Tissue Inhibitor of Metalloproteinase-1; D014746:Vimentin; D003094:Collagen; D020778:Matrix Metalloproteinase 2