Dataset Information

PBC-DIGE - Serological comparative proteomics analysis of mitochondrial autoantibody-negative and -positive primary biliary cirrhosis

ABSTRACT: DIGE combined with MALDI-TOF-TOF MS/MS was applied to explore the differential expressed proteins between AMA positive and negative PBC.
NB Extra peak files are available on the FTP for this project .

INSTRUMENT(S): 4800 Proteomics Analyzer

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Blood Serum

SUBMITTER: Chuiwen Deng

LAB HEAD: Chuiwen Deng

PROVIDER: PXD001397 | Pride | 2014-11-27

REPOSITORIES: Pride

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Publications

Serological comparative proteomics analysis of mitochondrial autoantibody-negative and -positive primary biliary cirrhosis.

Deng Chuiwen C Hu Chaojun C Wang Li L Zhang Shulan S Li Ping P Wu Ziyan Z Chen Si S Zhang Fengchun F Li Yongzhe Y

Electrophoresis 20150612 14

Here, we investigated the pathogenesis of primary biliary cirrhosis (PBC) by using 2D-DIGE to analyze serological differences between anti-mitochondrial antibody (AMA)-positive and -negative PBC patients. The study comprised 30 patients with PBC; 20 AMA-positive and ten AMA-negative patients matched for age, sex, and pathological stage. A screening group (four AMA-positive and four AMA-negative patients) was used for 2D-DIGE. Protein spots that were differently abundant between the two groups we ...[more]

PMID: 25875855

Similar Datasets

Project description:Primary biliary cirrhosis (PBC) is an immune-mediated chronic cholestatic liver disease with a slowly progressive course. Without treatment, most patients eventually develop fibrosis and cirrhosis of the liver and may need liver transplantation in the late stage of disease. PBC primarily affects women (female preponderance 9-10:1) with a prevalence of up to 1 in 1,000 women over 40 years of age. Common symptoms of the disease are fatigue and pruritus, but most patients are asymptomatic at first presentation. The diagnosis is based on sustained elevation of serum markers of cholestasis, i.e., alkaline phosphatase and gamma-glutamyl transferase, and the presence of serum antimitochondrial antibodies directed against the E2 subunit of the pyruvate dehydrogenase complex. Histologically, PBC is characterized by florid bile duct lesions with damage to biliary epithelial cells, an often dense portal inflammatory infiltrate and progressive loss of small intrahepatic bile ducts. Although the insight into pathogenetic aspects of PBC has grown enormously during the recent decade and numerous genetic, environmental, and infectious factors have been disclosed which may contribute to the development of PBC, the precise pathogenesis remains enigmatic. Ursodeoxycholic acid (UDCA) is currently the only FDA-approved medical treatment for PBC. When administered at adequate doses of 13-15 mg/kg/day, up to two out of three patients with PBC may have a normal life expectancy without additional therapeutic measures. The mode of action of UDCA is still under discussion, but stimulation of impaired hepatocellular and cholangiocellular secretion, detoxification of bile, and antiapoptotic effects may represent key mechanisms. One out of three patients does not adequately respond to UDCA therapy and may need additional medical therapy and/or liver transplantation. This review summarizes current knowledge on the clinical, diagnostic, pathogenetic, and therapeutic aspects of PBC.

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