Senescence marker protein 30 in acute liver failure: validation of a mass spectrometry proteomics assayReport as inadecuate




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BMC Gastroenterology

, 8:17

First Online: 28 May 2008Received: 03 January 2008Accepted: 28 May 2008

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.

Electronic supplementary materialThe online version of this article doi:10.1186-1471-230X-8-17 contains supplementary material, which is available to authorized users.

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Author: Sa Lv - Jiang-hua Wang - Feng Liu - Yan Gao - Ran Fei - Shao-cai Du - Lai Wei

Source: https://link.springer.com/







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