Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Deep vein thrombosis is one of the common complications of orthopedic surgery. Studies indicated that genetic factors played a considerable role in the pathogenesis of deep vein thrombosis. Endothelial nitric oxide synthase which encoded by nitric oxide synthase 3 (NOS3), can generate nitric oxide in endothelial cells. As a predominant regulator for vascular homeostasis, nitric oxide might be involved in the pathogenesis of thrombosis. It had been proved that the NOS3 polymorphism (rs1799983) was associated with the development of cardiovascular diseases. Our objective was to evaluate the association between the NOS3 polymorphism (rs1799983) and deep vein thrombosis after orthopedic surgery in Chinese Han population. The polymorphism was genotyped in 224 subjects with deep vein thrombosis after orthopedic surgery and 580 controls. Allele and genotype frequencies were compared between subjects with deep vein thrombosis and control subjects. The allele and genotype frequencies of the NOS3 polymorphism (rs1799983) were significantly different between subjects with deep vein thrombosis and control subjects. There were also significant differences when the subjects were stratified by gender, surgery type and hypertension status. These findings suggested that the NOS3 polymorphism (rs1799983) was associated with susceptibility to the deep vein thrombosis after orthopedic surgery in Chinese Han population, and NOS3 might play a role in the development of deep vein thrombosis after orthopedic surgery.
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PMID:Genetic polymorphism of NOS3 with susceptibility to deep vein thrombosis after orthopedic surgery: a case-control study in Chinese Han population. 2392 96

Endothelial nitric oxide synthase (eNOS) encoded by nitric oxide synthase 3 (NOS3), can generate nitric oxide (NO) which serves as an important deterrent to the pathogenesis of thrombosis by modulating the activation, adhesion and aggregate formation of platelets. Three serum miRNAs (miR-195, miR-532 and miR-582) have been suggested as biomarkers for the diagnosis of deep vein thrombosis (DVT), however their potential roles in DVT is not clear. The effect of miRNAs inhibiting the expression of NOS3 was evaluated in vitro. miR-195, miR-532 and miR-582 mimic, inhibitor, and control miRNAs were transfected into endothelial cells. The roles of miR-195, miR-532 and miR-582 regulating the expression of eNOS were evaluated by real-time quantitative PCR, Western Blotting and luciferase reporter assays. NO release was measured by Griess method. We confirmed NOS3 as a direct target of miR-195 and miR-582, which binds to the 3'-UTR of NOS3 mRNA in endothelial cells. A significantly inverse correlation between these two miRNAs and eNOS expression was detected. NO release from endothelial cells was decreased when the expression level of miR-195 and miR-582 was up-regulated. These findings indicated that miR-195 and miR-582 regulated NO release by targeting 3'-UTR of NOS3 post-transcriptionally in endothelial cells. Therefore, miR-195 and miR-582 might play an important role in maintaining endothelial NO bioavailability and could be a novel target for treatment of thrombotic diseases.
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PMID:microRNAs regulate nitric oxide release from endothelial cells by targeting NOS3. 2994 55

Endothelial progenitor cells are recognized as the potential targets for the revascularization and angiogenesis because of their ability to get themselves transformed into mature endothelial cells. Underlying pathophysiology in diabetes mellitus leads to decrease in circulatory endothelial progenitor cells, resulting in diabetic macro-vascular and micro-vascular complications. Peroxisome Proliferator Activated Receptor (PPAR) gamma analogues serves as an effective therapy for controlling blood sugar levels and preventing its complications. Reports of clinical trials and meta-analysis of clinical trial suggests the beneficial aspects of PPAR gamma therapy in increasing the number and function of circulating endothelial progenitor cells. This review highlights the pleotropic effect of PPAR gamma analogs, apart from their antidiabetic action via reduction of oxidative stress, increasing expression of eNOS, reducing level of miR 22, miR 222 levels and positive modulation of rapamycin/Protein kinase B/phosphoinoside3-kinase pathways, preventing the early apoptosis, enhanced mobility proliferation and transformation into mature endothelial cells. PPAR gamma therapy in diabetes regulates endothelial progenitor cells, reduces complications of diabetes like retinopathy, nephropathy, neuropathy, cardiomyopathy, deep vein thrombosis, and maintains the healthy vasculature.
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PMID:Potential role of Peroxisome Proliferator Activated Receptor gamma analogues in regulation of endothelial progenitor cells in diabetes mellitus: An overview. 3133 54