Alpha-syntrophin dependent expression of tubulin alpha 8 protein in hepatocytes

• Lisa Rein-Fischboeck ^[2] ; Ganimete Bajraktari ^[2] ; Rebekka Pohl ^[2] ; Susanne Feder ^[2] ; Kristina Eisinger ^[2] ; Wolfgang Mages ^[1] ; Elisabeth M. Haberl ^[2] ; Christa Buechler ^[2]
  1. [1] University of Regensburg

     University of Regensburg

     Kreisfreie Stadt Regensburg, Alemania

     
  2. [2] Regensburg University Hospital, Alemania
• Localización: Journal of physiology and biochemistry, ISSN-e 1877-8755, ISSN 1138-7548, Vol. 74, Nº. 4 (November 2018), 2018 (Ejemplar dedicado a: CTPIOD meeting (Contribution To Progress in Obesity and Diabetes Research) 2017 / Fermín Ignacio Milagro Yoldi (ed. lit.), Christian Carpéné (ed. lit.)), págs. 511-521
• Idioma: inglés
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• Resumen

  • The scaffold protein alpha-syntrophin (SNTA) is a component of the dystrophin glycoprotein complex and has been comprehensively studied in skeletal muscle and adipocytes. SNTA is further expressed in the liver where its biological role remains unclear. Unpublished data from our group suggested that SNTA deficiency is associated with altered tubulin alpha 8 (TUBA8) levels in fat. TUBA8 is highly expressed in different cell lines including hepatoma cells, and here we analyzed whether SNTA has a role herein. In Hepa1-6 cells, TUBA8 protein levels were increased upon SNTA knock down and were reduced upon overexpression of SNTA. This regulation was not identified when analyzing mRNA expression. In the liver of SNTA-deficient mice, TUBA8 protein was higher compared to the respective wild-type controls while RNA expression was even suppressed. Using the HaloTag platform, TUBA8 was found to form a complex with SNTA in Hepa1-6 cells. In the hepatic stellate cell line LX-2, the lack or overexpression of SNTA did, however, not change TUBA8 protein expression. SNTA and TUBA8 are described to regulate cell proliferation. Yet, knock down of SNTA did neither affect proliferation nor viability of Hepa1-6 cells. The present study shows that SNTA protein levels are inversely related to TUBA8 protein expression in the hepatocyte cell line Hepa1-6.