BIOMAT Database Logo BIOMAT Database Logo

Hepatic alpha 1-antitrypsin mRNA content in cirrhosis with normal and abnormal protease inhibitor phenotypes. 1986

S J Schwarzenberg, and H L Sharp, and R D Manthei, and S Seelig

We quantitated alpha 1-antitrypsin mRNA in normal, alpha 1-antitrypsin-deficient cirrhotic and biliary cirrhotic livers using two-dimensional electrophoretograms of [35S]methionine-labeled translational products of total hepatic RNA and RNA/DNA hybridization. alpha 1-Antitrypsin precursor product was identified by immunoprecipitation. The relative abundance of alpha 1-antitrypsin product from normal (0.989 +/- 0.197), cirrhotic (0.956 +/- 0.062) and alpha 1-antitrypsin deficient (0.818 +/- 0.12) livers was not significantly different. Although (RNA/DNA) was decreased in the PiZZ cirrhotic livers compared to normal (0.56 +/- 0.045 vs. 0.95 +/- 0.225), it equaled that found in the PiM cirrhotic livers (0.56 +/- 0.055). The concentration of alpha 1-antitrypsin mRNA [relative abundance X (RNA/DNA)], while decreased in PiZZ compared to normal liver, is thus no different in PiZZ cirrhotics than in PiM cirrhotics. We confirmed this observation by quantitation of the alpha 1-antitrypsin mRNA using an alpha 1-antitrypsin genomic probe. By RNA/DNA hybridization, alpha 1-antitrypsin mRNA was equal in PiM cirrhotic and PiZZ cirrhotic (38.48 +/- 4.5 vs. 31.93 +/- 2.1), but significantly decreased from noncirrhotic PiM liver (58.36 +/- 12.7). We conclude that alpha 1-antitrypsin mRNA is decreased in cirrhosis of any etiology, and this decrease appears to represent a general response of the liver to injury. Since the decreased alpha 1-antitrypsin mRNA in PiM cirrhotics is associated with normal serum alpha 1-antitrypsin levels, it is unlikely that the decreased alpha 1-antitrypsin mRNA in PiZZ cirrhotics accounts for their decreased serum levels.

UI MeSH Term Description Entries
D007223 Infant A child between 1 and 23 months of age. Infants
D008099 Liver A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances. Livers
D008103 Liver Cirrhosis Liver disease in which the normal microcirculation, the gross vascular anatomy, and the hepatic architecture have been variably destroyed and altered with fibrous septa surrounding regenerated or regenerating parenchymal nodules. Cirrhosis, Liver,Fibrosis, Liver,Hepatic Cirrhosis,Liver Fibrosis,Cirrhosis, Hepatic
D009693 Nucleic Acid Hybridization Widely used technique which exploits the ability of complementary sequences in single-stranded DNAs or RNAs to pair with each other to form a double helix. Hybridization can take place between two complimentary DNA sequences, between a single-stranded DNA and a complementary RNA, or between two RNA sequences. The technique is used to detect and isolate specific sequences, measure homology, or define other characteristics of one or both strands. (Kendrew, Encyclopedia of Molecular Biology, 1994, p503) Genomic Hybridization,Acid Hybridization, Nucleic,Acid Hybridizations, Nucleic,Genomic Hybridizations,Hybridization, Genomic,Hybridization, Nucleic Acid,Hybridizations, Genomic,Hybridizations, Nucleic Acid,Nucleic Acid Hybridizations
D010641 Phenotype The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment. Phenotypes
D002648 Child A person 6 to 12 years of age. An individual 2 to 5 years old is CHILD, PRESCHOOL. Children
D002675 Child, Preschool A child between the ages of 2 and 5. Children, Preschool,Preschool Child,Preschool Children
D004247 DNA A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine). DNA, Double-Stranded,Deoxyribonucleic Acid,ds-DNA,DNA, Double Stranded,Double-Stranded DNA,ds DNA
D004586 Electrophoresis An electrochemical process in which macromolecules or colloidal particles with a net electric charge migrate in a solution under the influence of an electric current. Electrophoreses
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man

Related Publications

S J Schwarzenberg, and H L Sharp, and R D Manthei, and S Seelig
Alpha-1-antitrypsin (protease inhibitor) phenotypes and longevity.
January 1990, Human heredity,
S J Schwarzenberg, and H L Sharp, and R D Manthei, and S Seelig
Antitrypsin deficiency and abnormal protease inhibitor phenotypes.
September 1973, Archives of environmental health,
S J Schwarzenberg, and H L Sharp, and R D Manthei, and S Seelig
Alpha-1-antitrypsin protease inhibitor SZ phenotype and liver cirrhosis.
January 1989, Applied pathology,
S J Schwarzenberg, and H L Sharp, and R D Manthei, and S Seelig
Alpha-I-antitrypsin phenotypes in adult hepatic cirrhosis.
July 1976, Irish medical journal,
S J Schwarzenberg, and H L Sharp, and R D Manthei, and S Seelig
[Alpha-1-antitrypsin and hepatic cirrhosis].
February 1986, Revista espanola de las enfermedades del aparato digestivo,
S J Schwarzenberg, and H L Sharp, and R D Manthei, and S Seelig
Alpha 1-antitrypsin phenotypes in cirrhosis and hepatoma.
April 1976, Acta hepato-gastroenterologica,
S J Schwarzenberg, and H L Sharp, and R D Manthei, and S Seelig
Alpha-1-antitrypsin protease inhibitor (Pi) phenotypes in Down's syndrome patients and their parents.
January 1982, Clinical genetics,
S J Schwarzenberg, and H L Sharp, and R D Manthei, and S Seelig
Alpha-1-protease inhibitor phenotypes in Australia.
January 1982, Human heredity,
S J Schwarzenberg, and H L Sharp, and R D Manthei, and S Seelig
Protease inhibitor phenotypes and serum alpha-1-antitrypsin levels in patients with COPD: a study from Hong Kong.
June 2004, Respirology (Carlton, Vic.),
S J Schwarzenberg, and H L Sharp, and R D Manthei, and S Seelig
[Substitution therapy in alpha 1-protease inhibitor deficiency (alpha 1-antitrypsin deficiency)].
November 1991, Schweizerische Rundschau fur Medizin Praxis = Revue suisse de medecine Praxis,
Copied contents to your clipboard!