The adaptor protein alpha-syntrophin is reduced in human non-alcoholic steatohepatitis but is unchanged in hepatocellular carcinoma

Rein-Fischboeck, Lisa and Pohl, Rebekka and Haberl, Elisabeth M. and Weiss, Thomas S. and Buechler, Christa (2017) The adaptor protein alpha-syntrophin is reduced in human non-alcoholic steatohepatitis but is unchanged in hepatocellular carcinoma. EXPERIMENTAL AND MOLECULAR PATHOLOGY, 103 (2). pp. 204-209. ISSN 0014-4800, 1096-0945

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Abstract

The adaptor protein alpha-syntrophin (SNTA) is differentially expressed in varying types of cancer and affects triglyceride levels, inflammatory response and cell proliferation. However, little is known about the expression of SNTA in liver diseases. Non-alcoholic steatohepatitis (NASH) is characterized by hepatic steatosis, inflammation and eventually fibrosis, and may progress to hepatocellular carcinoma (HCC). Here, SNTA mRNA was analyzed in liver tissues from 71 non-alcoholic fatty liver disease patients and 32 controls to assess associations with disease characteristics. SNTA mRNA expression was reduced in NASH liver and negatively correlated with steatosis, inflammation, fibrosis and NASH scores. In the NASH patients, those with type 2 diabetes had a higher fibrosis score, reduced inflammation and increased hepatic SNTA mRNA levels demonstrating a strong association of SNTA mRNA levels with inflammation. Recently, we have shown diminished expression of the high-density lipoprotein scavenger receptor BI (SR-BI) in the liver of syntrophin-deficient mice. Indeed, hepatic SNTA and SR-BI mRNA were positively correlated. SNTA protein was further determined in tumor and non-tumorous tissues of 21 HCC patients. Protein expression was unchanged in the tumor and not related to staging and grading. Present study identified associations of hepatic SNTA mRNA levels with SR-BI and features of NASH assuming a function of this protein in chronic liver disease and cholesterol metabolism.

Item Type: Article
Uncontrolled Keywords: FATTY LIVER-DISEASE; NITRIC-OXIDE SYNTHASE; HEPATIC STELLATE CELLS; SR-BI; APOA-I; MICE; ABCA1; INFLAMMATION; AQUAPORIN-4; UTROPHIN; Inflammation; Type 2 diabetes; SR-BI; Malignancy
Subjects: 600 Technology > 610 Medical sciences Medicine
Divisions: Medicine > Lehrstuhl für Innere Medizin I
Medicine > Lehrstuhl für Kinder- und Jugendmedizin
Depositing User: Dr. Gernot Deinzer
Date Deposited: 14 Dec 2018 13:19
Last Modified: 19 Feb 2019 13:59
URI: https://pred.uni-regensburg.de/id/eprint/2054

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