title: Deletion of SIP1 promotes liver regeneration and lipid accumulation.
abstract: BACKGROUND
  The function of Smad interacting protein-1 (SIP1) in liver regeneration is not yet known. As it is a key factor linked to the TGF-β, BMP and Wnt signaling pathways, which are important for liver regeneration, we tested whether SIP1 might also have a critical role in liver regeneration after liver injury.
  
  
  METHODS
  In this study, the 2/3 partial hepatectomy (2/3 PH) animal model was used to assess wild-type and SIP1 tissue-specific knockout mice. We collected the blood and liver tissue at selected time points after inducing injury. The level of liver regeneration was monitored using several methods, including H&E staining, immunohistochemistry (IHC), Western blotting, and qPCR.
  
  
  RESULTS
  There was no difference between adult SIP1 knockout and wild-type mice in morphological appearance or liver tissue sections. The peak level of BrdU- and Ki67-positive cells was observed at 36h after PH in both SIP1 knockout and wild-type mice. However, the peak level of BrdU- and Ki67-positivity was higher in SIP1 knockout mice than in wild-type mice (P<0.05). A higher amount of peak cyclin protein expression was also observed in SIP1 knockout mice. Furthermore, lipid accumulation was observed in SIP1 knockout mice during the liver regeneration process. Expression of Plin2, which plays an essential role in adipose differentiation, was found to be significantly higher in SIP1 knockout mice than in wild-type mice after 2/3 PH (P<0.05).
  
  
  CONCLUSIONS
  SIP1 plays an essential role in lipid metabolism during the liver regeneration process and might be a regulator of liver regeneration following PH injury.
authors.affiliation: Laboratory of Pathology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China; Department of Pathology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China.
authors.forename: Libo
authors.initials: L
authors.lastname: Yang
authors.affiliation: Laboratory of Pathology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China.
authors.forename: Yujia
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Laboratory of Pathology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China.
authors.forename: Yujun
authors.initials: Y
authors.lastname: Shi
authors.affiliation: Laboratory of Pathology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China; Department of Pathology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China.
authors.forename: Hong
authors.initials: H
authors.lastname: Bu
authors.affiliation: Laboratory of Pathology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China. Electronic address: fengye@scu.edu.cn.
authors.forename: Feng
authors.initials: F
authors.lastname: Ye
mesh_terms: D000818:Animals; D002454:Cell Differentiation; D004195:Disease Models, Animal; D006498:Hepatectomy; D008055:Lipids; D008099:Liver / Q000293:injuries* / Q000378:metabolism*; D008115:Liver Regeneration / Q000235:genetics*; D051379:Mice; D018345:Mice, Knockout; D009419:Nerve Tissue Proteins / Q000235:genetics* / Q000378:metabolism; D000070780:Perilipin-2 / Q000235:genetics / Q000378:metabolism
chemical_list: D008055:Lipids; D009419:Nerve Tissue Proteins; D000070780:Perilipin-2; C000602983:Plin2 protein, mouse; C491561:Sip1 protein, mouse
keywords: Lipid metabolism; Liver injury; Liver regeneration; SIP1