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Int J Clin Exp Pathol 2011;4(7):661-666
Increased expression of Zinc finger protein 267 in non-alcoholic fatty liver disease
Bernd Schnabl, Barbara Czech, Daniela Valletta, Thomas S Weiss, Georgi Kirovski, and Claus Hellerbrand
Department of Internal Medicine I, University Hospital Regensburg, Germany, Department of Medicine, University of California San Diego, La
Jolla, CA, USA, Center for Liver Cell Research, Department of Pediatrics and Juvenile Medicine, University Hospital Regensburg, Germany.
Received August 25, 2011; accepted September 10, 2011; Epub September 22, 2011; published October 31, 2011
Abstract: Hepatocellular lipid accumulation is a hallmark of non-alcoholic fatty liver disease (NAFLD), which encompasses a spectrum
ranging from simple steatosis to non-alcoholic steatohepatitis (NASH) and ultimately cirrhosis. Zinc finger protein 267 (ZNF267) belongs to the
family of Kruppel-like transcription factors, which regulate diverse biological processes that include development, proliferation, and
differentiation. We have previously demonstrated that ZNF267 expression is up-regulated in liver cirrhosis and is further increased in
hepatocellular carcinoma (HCC). Here, we analyzed the expression of ZNF267 in tissue specimens of NAFLD patients and found a significant
up-regulation compared to normal liver tissue. Noteworthy, ZNF267 mRNA was already significantly increased in steatotic liver tissue without
inflammation. In line with this, incubation of primary human hepatocytes with palmitic acid induced a dose-dependent lipid accumulation and
corresponding dose-dependent ZNF267 induction in vitro. Furthermore, hepatocellular lipid accumulation induced formation of reactive oxygen
species (ROS), and also chemically induced ROS formation increased ZNF267 mRNA expression. In summary with previous findings, which
revealed ZNF267 as pro-fibrogenic and pro-cancerogenic factor in chronic liver disease, the present study further suggests ZNF267 as
promising therapeutic target particularly for NAFLD patients. In addition, it further indicates that hepatic steatosis per se has pathophysiological
relevance and should not be considered as benign. (IJCEP1108019).
Keywords: Non-alcoholic fatty liver disease, Kruppel-like factor, ZNF267
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Address all correspondence to:
Dr. Claus Hellerbrand
University Hospital Regensburg, Department of Internal Medicine I
D-93042 Regensburg, Germany.
Tel: +49-941-944-7155, Fax: +49-941-944-7154