Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vascular smooth muscle cells (VSMCs) from spontaneously hypertensive rats (SHR) show the synthetic phenotype and exaggerated growth in comparison with VSMCs from normotensive Wistar-Kyoto (WKY) rats. We investigated genes associated with the synthetic phenotype and exaggerated growth of VSMCs from SHR by microarray. Expression of 1300 transcripts was evaluated by microarray with total mRNA extracted from mid-layer aortic smooth muscle of 3-week-old SHR/Izumo and WKY/Izumo rats. mRNAs encoding sodium-dependent neurotransmitter transporter, epidermal growth factor precursor, EEF2, leptin receptor long-isoform b, clathrin assembly protein short form, and preprocomplement 3 (pre-pro-C3) were expressed only in aortic smooth muscle from SHR by microarray and by reverse-transcription polymerase chain reaction analysis. Pre-pro-C3 mRNA was detected only in cultured VSMCs from SHR. Exogenous C3 changed VSMCs to the synthetic phenotype. Antisense oligodeoxynucleotides (ODN) to C3 reduced the higher level of DNA synthesis in VSMCs from SHR. Antisense ODN to C3 increased expression of SM22alpha mRNA and decreased expression of osteopontin and matrix Gla mRNAs. It also decreased expression of growth factor mRNAs in VSMCs from SHR. In conclusion, we have shown that C3, independent of other complement molecules, has direct effects on the phenotype of VSMCs and stimulates growth of these cells. C3 is produced only by VSMCs from SHR. Therefore, C3 may be the gene underlying the synthetic phenotype and exaggerated growth of VSMCs from SHR. C3 may be a new target for the treatment of hypertension.
Hypertension 2004 Jul
PMID:Complement 3 is involved in the synthetic phenotype and exaggerated growth of vascular smooth muscle cells from spontaneously hypertensive rats. 1512 74

In the past decade, the small polyphenol resveratrol has received widespread attention as either a potential therapy or as a preventive agent for numerous age-related chronic diseases, including cardiovascular atherosclerosis, cancer, hypertension, and diabetes, but the biological processes and molecular pathways by which resveratrol induces these beneficial effects, as well as its safety and toxicology remain largely undefined. To explore the molecular mechanisms of resveratrol involved in the amelioration of endothelial dysfunction and vascular disease, in the present study the protein profile changes of human umbilical vein endothelial cells in response to resveratrol treatment were investigated using proteomics approaches (2-DE combined with MS/MS). As a result, four down-regulated protein species named elongation factor 2 (EEF2), carboxymethyl-cofilin-1 (cofilin-1), acetyl-eukaryotic translation initiation factor 5A-1 (acetyl-EIF5A) and barrier-to-autointegration factor, and five up-regulated protein species named heat shock protein beta-1 (HSP27), phospho-HSP27, phospho-stathmin, Nicotinate-nucleotide pyrophosphorylase and 1,2-dihydroxy-3-keto-5-methylthiopentene dioxygenase were identified. Among them, two translation-related protein species (EEF2 and acetyl-EIF5A) were the most significantly changed (over tenfold). Phospho-EEF2 was further verified to be dramatically up-regulated by immunoblot assays. It is notable that in the present study several protein species with post-transcriptional modification (carboxymethyl-, acetyl-, and phospho-) were found to be altered following exposure to resveratrol. These findings may improve our understanding of the molecular mechanisms underlying the pleiotropic effects of resveratrol on endothelial cells.
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PMID:Proteomics analysis of human umbilical vein endothelial cells treated with resveratrol. 2234 66