Abstract
BackgroundOur previous proteomic study showed that the senescence marker protein (SMP30) is selectively present in the plasma of a murine model of acute liver failure (ALF). The aim of this study was to validate this SMP30 expression in the plasma and liver tissues of mice and humans with ALF.MethodsAfter the proteomic analysis of plasma from a murine model of D-galactosamine/lipopolysaccharide (GalN/LPS)-induced ALF by two-dimensional electrophoresis (2-DE) and mass spectrometry, the expression levels of SMP30 in the plasma and liver tissues were validated by western blot and RT-PCR analyses. These results were then confirmed in plasma samples from humans.ResultsThese data validate the results of 2-DE, and western blot showed that SMP30 protein levels were only elevated in the plasma of ALF mice. Further analysis revealed that GalN/LPS induced the downregulation of SMP30 protein levels in liver tissues (by approximately 25% and 16% in the GalN/LPS-treated mice and in the treated mice that survived, respectively; P < 0.01). Hepatic SMP30 mRNA levels decreased by about 90% only in the mice that survived the GalN/LPS treatment. Importantly, plasma obtained from patients with ALF also contained higher levels of SMP30, about (3.65 ± 0.34) times those observed in healthy volunteers.ConclusionThis study shows that SMP30 is not only a potential biomarker for the diagnosis and even prognosis of ALF. It also plays a very important role in a self-protective mechanism in survival and participates in the pathophysiological processes of ALF.
Highlights
Our previous proteomic study showed that the senescence marker protein (SMP30) is selectively present in the plasma of a murine model of acute liver failure (ALF)
BMC Gastroenterology 2008, 8:17 http://www.biomedcentral.com/1471-230X/8/17 teomic analysis with two-dimensional electrophoresis (2DE) and mass spectrometry, we identified 10 protein molecules with altered expression in the plasma of ALF mice [5]
senescence marker protein 30 (SMP30) only elevated in plasma of ALF mice according to 2-DE Coinjection of GalN/LPS successfully induced the ALF animal model and about 10% of these mice survived
Summary
Our previous proteomic study showed that the senescence marker protein (SMP30) is selectively present in the plasma of a murine model of acute liver failure (ALF). The aim of this study was to validate this SMP30 expression in the plasma and liver tissues of mice and humans with ALF. Comparative proteomics has provided new insights into the mechanisms and processes of liver disease. Many candidate biomarkers have been discovered that are associated with hepatocarcinoma, viral hepatitis, or liver cirrhosis [1,2,3,4]. The proteins identified in these studies should be examined by other techniques to confirm their expression patterns. Because many studies involve animal experiments, their results should be validated in human samples. We established a murine model of acute liver failure (ALF) by the administration of D-galactosamine/lipopolysaccharide (GalN/LPS).
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