The mechanism of liver atrophy after portal vein hypoperfusion and therapeutic method using LSKL peptide

2016 Fiscal Year Final Research Report

• Project/Area Number: 26462046
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Digestive surgery
• Research Institution: Kumamoto University
• Principal Investigator: IKUTA Yoshiaki 熊本大学, 医学部附属病院, 非常勤診療医師 (70452894)
• Research Collaborator: KUROKI Hideyuki 熊本大学, 医学部附属病院, 非常勤診療医師 (50594876) ; MIYAKE Keisuke 熊本大学, 大学院生命科学研究部(医), リサーチスペシャリスト
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 門脈血流低下 / 肝萎縮 / TSP-1 / 肝細胞増殖抑制 / 肝細胞アポトーシス誘導

Outline of Final Research Achievements

Liver atrophy was induced right portal vein ligation of wild type mouse. PCNA expression elevated at 6 hour after portal vein ligation and decreased thereafter in ligated liver (atrophic liver). TUNEL stained nuclei in liver cells increased over time. TSP-1 expression in cytoplasm of ligated liver increased since 6 hour after portal vein ligation. cDNA microarray assay was performed on ligated and non-ligated human liver for therapeutic hepatectomy. TSP-1 was most induced among 132 genes in ligated liver than in none ligated liver.
These results show hypoperfusion of portal vein induce TSP-1 expression in hepatocyte and suppress proliferation and induce apoptosis of hepatocyte.

Free Research Field

肝胆膵外科