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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Corrales, F. J. Kanel, G. Alvarez, L. An, W. Chen, L. Huang, Z. Z. Avila, M. A. Lu, S. C. Mato, J. M. |
| Description | Author Affiliation: Lu SC ( Liver Disease Research Center, Research Center for Alcoholic Liver and Pancreatic Diseases, University of Southern California-University of California, Los Angeles, CA 90033, USA. shellylu@hsc.usc.edu); |
| Abstract | Liver-specific and nonliver-specific methionine adenosyltransferases (MATs) are products of two genes, MAT1A and MAT2A, respectively, that catalyze the formation of S-adenosylmethionine (AdoMet), the principal biological methyl donor. Mature liver expresses MAT1A, whereas MAT2A is expressed in extrahepatic tissues and is induced during liver growth and dedifferentiation. To examine the influence of MAT1A on hepatic growth, we studied the effects of a targeted disruption of the murine MAT1A gene. MAT1A mRNA and protein levels were absent in homozygous knockout mice. At 3 months, plasma methionine level increased 776% in knockouts. Hepatic AdoMet and glutathione levels were reduced by 74 and 40%, respectively, whereas S-adenosylhomocysteine, methylthioadenosine, and global DNA methylation were unchanged. The body weight of 3-month-old knockout mice was unchanged from wild-type littermates, but the liver weight was increased 40%. The Affymetrix genechip system and Northern and Western blot analyses were used to analyze differential expression of genes. The expression of many acute phase-response and inflammatory markers, including orosomucoid, amyloid, metallothionein, Fas antigen, and growth-related genes, including early growth response 1 and proliferating cell nuclear antigen, is increased in the knockout animal. At 3 months, knockout mice are more susceptible to choline-deficient diet-induced fatty liver. At 8 months, knockout mice developed spontaneous macrovesicular steatosis and predominantly periportal mononuclear cell infiltration. Thus, absence of MAT1A resulted in a liver that is more susceptible to injury, expresses markers of an acute phase response, and displays increased proliferation. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 10 |
| Volume Number | 98 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2001-05-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Cell Division Genetics Gene Expression Regulation, Enzymologic Genetic Predisposition To Disease Liver Cirrhosis, Experimental Methionine Adenosyltransferase Physiology Animals DNA Methylation Disease Models, Animal Liver Metabolism Methionine Blood Mice Mice, Knockout Phenotype Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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