Open AccessCaspase‐cleaved cytokeratin 18 and 20 S proteasome in liver degeneration
Author(s) -
Hetz Hubert,
Hoetzenecker Konrad,
Hacker Stefan,
Faybik Peter,
Pollreisz Andreas,
Moser Bernhard,
Roth Georg,
Hoetzenecker Wolfram,
Lichtenauer Michael,
Klinger Markus,
Krenn Claus Georg,
Ankersmit Hendrik Jan
Publication year - 2007
Publication title -
journal of clinical laboratory analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 50
eISSN - 1098-2825
pISSN - 0887-8013
DOI - 10.1002/jcla.20180
Subject(s) - cytokeratin , proteasome , apoptosis , caspase , medicine , primary biliary cirrhosis , cirrhosis , caspase 3 , population , pathology , endocrinology , biology , immunohistochemistry , programmed cell death , biochemistry , environmental health
Apoptosis of epithelial hepatocytes plays a pivotal role in acute as well as in chronic liver diseases. The cleavage of cytokeratin‐18 (CK‐18) by caspases is an early event in the apoptotic process. We therefore sought to investigate serum levels of CK‐18 and 20S proteasome in patients with liver cirrhosis, primary graft dysfunction (PDF), and acute liver failure (ALF), and in healthy volunteers. Enzyme‐linked immunosorbent assay (ELISA) was utilized to measure the concentration of M30, a fragment of CK‐18 cleaved at Asp396 (M30 neoantigen), and the concentration of 20S proteasome. Serum levels of the CK‐18 neoepitope M30 were significantly increased in ALF, primary graft dysfunction, and liver cirrhosis vs. healthy controls (1,993.6±124.7 U/L, 2,238.1±235.9 U/L, and 673.6±86.5 U/L vs. 66.8±29.1 U/L, respectively, P <0.001). Similar results were detected with the evaluation of 20S proteasome (124,014.5±13,235.6 ng/mL, 76,993.2±15,720.1 ng/mL, and 2,395.9±1,098.2 ng/mL vs. 1,074.5±259.4 ng/mL, respectively; P <0.001). Detection of CK‐18 neoepitope M30 and 20S proteasome may represent a novel marker of tracing apoptotic epithelium, respectively mirroring degenerative liver processes in affected patient population. J. Clin. Lab. Anal. 21:277–281, 2007. © 2007 Wiley‐Liss, Inc.