TY - JOUR
T1 - Prenatal ethanol exposure alters the cytoskeleton and induces glycoprotein microheterogeneity in rat newborn hepatocytes
AU - Azorín, Inmaculada
AU - Portolés, Manuel
AU - Marín, Pilar
AU - Lázaro-Diéguez, Francisco
AU - Megías, Luis
AU - Egea, Gustavo
AU - Renau-Piqueras, Jaime
N1 - Funding Information:
Acknowledgements — This work is supported by grants from MCyT (SAF2000-0042 to G.E. and BFI2001-0123-CO2-02 to G.E. and J. R-P.) and FIS (PI020073 to J.R.-P.). M.T. and P.M. are recipients of pre-doctoral fellowships from FIS and CIEN Programme C03/176 (FIS), respectively, and F.L.-D. is a recipient of a pre-doctoral fellowships from IDIBAPS. The authors thank Dr Consuelo Guerri for providing control and alcohol-exposed animals and his comments on the manuscript, and to Robin Rycroft for improving the English of the text of this article.
PY - 2004/5
Y1 - 2004/5
N2 - Aims: Prenatal ethanol exposure (PEA) increases both liver weight and total protein content in the Golgi complex and alters its morphological and functional properties. As PEA-induced protein retention could be the synergetic consequence of alterations in the cytoskeleton and in the glycan biosynthesis, and there are no data that in liver PEA perturbs the cytoskeleton, we examined in hepatocytes whether PEA affects the main cytoskeleton elements. We also analysed whether ethanol induces glycoprotein microheterogeneity by altering the sugar composition of glycoproteins. Methods: Livers from 0-day newborn control and PEA rats were used. The carbohydrate moiety of glycoproteins was determined by lectin blotting. The content and intracellular distribution of cytoskeleton proteins was analysed using immunoblotting, immunofluorescence and immunogold. Results: PEA delayed the post-Golgi transport of albumin but not of transferrin. PEA also increased the levels of cytokeratin and tubulin, but it decreased the amount of tubulin capable of assembling into functional microtubules. PEA perturbed the distribution of cytokeratin and tubulin and induced microheterogeneity in several glycoproteins. Conclusions: PEA-induced retention of proteins in fetal hepatocytes could be the result of an alteration of glycoprotein biosynthesis and cytoskeleton-mediated transport.
AB - Aims: Prenatal ethanol exposure (PEA) increases both liver weight and total protein content in the Golgi complex and alters its morphological and functional properties. As PEA-induced protein retention could be the synergetic consequence of alterations in the cytoskeleton and in the glycan biosynthesis, and there are no data that in liver PEA perturbs the cytoskeleton, we examined in hepatocytes whether PEA affects the main cytoskeleton elements. We also analysed whether ethanol induces glycoprotein microheterogeneity by altering the sugar composition of glycoproteins. Methods: Livers from 0-day newborn control and PEA rats were used. The carbohydrate moiety of glycoproteins was determined by lectin blotting. The content and intracellular distribution of cytoskeleton proteins was analysed using immunoblotting, immunofluorescence and immunogold. Results: PEA delayed the post-Golgi transport of albumin but not of transferrin. PEA also increased the levels of cytokeratin and tubulin, but it decreased the amount of tubulin capable of assembling into functional microtubules. PEA perturbed the distribution of cytokeratin and tubulin and induced microheterogeneity in several glycoproteins. Conclusions: PEA-induced retention of proteins in fetal hepatocytes could be the result of an alteration of glycoprotein biosynthesis and cytoskeleton-mediated transport.
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U2 - 10.1093/alcalc/agh043
DO - 10.1093/alcalc/agh043
M3 - Article
C2 - 15082457
AN - SCOPUS:2342535877
SN - 0735-0414
VL - 39
SP - 203
EP - 212
JO - Alcohol and Alcoholism
JF - Alcohol and Alcoholism
IS - 3
ER -
