Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperhomocysteinemia is a common independent risk factor for cardiovascular diseases. The promoting effect of homocysteine (Hcy) on vascular smooth muscle cell (VSMC) proliferation has been considered as one of the important pathological bases of atherosclerosis. However, the mechanism of VSMC proliferation induced by Hcy remains unclear. The present research used proteomic techniques to globally analyze the protein changes in proliferative VSMCs. After comparing the protein expression profiles of VSMCs between the Hcy-treated and non-treated groups, 11 protein spots were found altered markedly in proliferative VSMCs with expression of eight protein spots increased and three protein spots decreased. In the differentially expressed proteins, eight protein spots were identified successfully including glycolytic metabolism proteins: pyruvate kinase M2 (PKM2), triosephosphate isomerase (TPI) and aldose reductase (AR); cytoskeletal proteins: lamin C and vimentin; and three other proteins: calreticulin; similar to WDR1 protein and LIM and SH3 protein 1. The differentially expressed proteins were further validated by Western blot and confirmed by assay of enzymes' activities and ATP content. These results may provide some clues for comprehensively understanding the mechanism of VSMC proliferation and pathogenesis of atherosclerosis induced by Hcy.
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PMID:Proteomic analysis of homocysteine induced proliferation of cultured neonatal rat vascular smooth muscle cells. 1903 67

Smoking accelerates atherosclerosis and is a well-known risk factor for acute cardiovascular complications; however, the mechanisms of these effects have not been completely clarified. Recently developed proteomic approaches may offer new clues when combined with well-established functional tests. Platelet proteome of healthy smokers and non-smokers was resolved by two-dimensional difference gel electrophoresis, compared by Decyder software and identified by mass spectrometry analysis (nano-LC-MS/MS). In smokers, three proteins (Factor XIII-A subunit, platelet glycoprotein IIb and beta-actin) were significantly up-regulated, whereas WDR1 protein and chaperonine HSP60 were down-regulated. Furthermore, the highest scored network derived by Ingenuity Pathway Analysis using the modulated proteins as input showed the involvement of several proteins to be related to inflammation and apoptosis. Platelet function tests and the levels of markers of platelet and leukocyte activation were not different in smokers vs. non-smoker subjects. The platelet proteomic approach confirms that cigarette smoking triggers several inflammatory reactions and may help clarify some of the molecular mechanisms of smoke effect on cellular systems relevant for vascular integrity and human health.
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PMID:Platelet proteome in healthy volunteers who smoke. 2173 19