Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.7.48 (transcriptase)
 9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Avian thrombocytes are nucleated blood cells homologous in function to mammalian platelets. In the present study, we obtained a cDNA from chicken thrombocyte polyadenylated RNA [Poly(A)+RNA], which coded for the chicken PDGF-B chain. The sequence was 1083-bp long and had an open reading frame (ORF) of 753-bp. At the amino acid level, the predicted mature protein showed 69% homology with the processed coding region of human PDGF-B. Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis showed that PDGF-B mRNA was expressed at high levels in thrombocytes and in the lung. The expression of PDGF-B chain mRNA in thrombocytes reached its maximum level 12h following type 1 collagen treatment. These results suggest that chicken PDGF-B chain may play an important role in the vascular system and in healing wounded tissue.
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PMID:Cloning and characterization of a chicken platelet-derived growth factor B-chain cDNA. 1168 65

Smooth muscle cell (SMC) proliferation and intimal thickening are hallmark features of atherosclerotic disease, and Chlamydia pneumoniae may contribute to atherogenesis by imparting biological effects on SMCs. An in vitro endothelial cell model and a normocholesterolemic rabbit model were used to test the hypothesis that infection with C. pneumoniae induces SMC growth factor production, SMC proliferation, and aortic intimal thickening. Using reverse-transcriptase polymerase chain reaction, it was demonstrated that C. pneumoniae infection of endothelial cells induced platelet-derived growth factor (PDGF)-B messenger RNA expression. In C. pneumoniae-infected rabbits, maximum intimal thickness (MIT) was significantly greater than that in uninfected animals (P< .0001). MIT correlated with the presence of C. pneumoniae antigen (P= .043) and PDGF-B (P= .002) in aortic tissues, and C. pneumoniae antigen was independently correlated with the presence of PDGF-B in aortic tissues (P= .009). These results suggest that C. pneumoniae-induced SMC proliferation and intimal thickening may be mediated through PDGF-B and may be a molecular mechanism by which C. pneumoniae infection could contribute to atherogenesis.
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PMID:Chlamydia pneumoniae infection of endothelial cells induces transcriptional activation of platelet-derived growth factor-B: a potential link to intimal thickening in a rabbit model of atherosclerosis. 1202 68

Chronic decubital lesions have a limited potential to heal. Evidence suggests that a lack of local revascularization is involved in this aetiology. The present study investigated the expression of one of the most important angiogenic factors, the vascular endothelial growth factor (VEGF), in different regions of sacral chronic decubital lesions and in normal skin by immunohistochemical, biochemical, molecular, and cell biology methods. To elucidate some of the factors responsible for the induction of VEGF in chronic skin ulcers, cultured fibroblasts were exposed to hypoxia and/or growth factors. In the central part (zone I) of chronic ulcers and in normal skin, immunostaining for VEGF remained largely negative. However, VEGF could be immunostained in cells in the granulation tissue adjacent to central necrosis (zone II). VEGF receptor 2 (VEGFR-2; KDR) could also be identified in microvessels. High VEGF levels were present in homogenates from granulation tissue by enzyme-linked immunosorbent assay (ELISA) and western blot experiments: low concentrations were found in areas of central necrosis and negligible amounts were present in normal skin. Reverse transcriptase-polymerase chain reaction (RT-PCR) showed that only the splice variants VEGF(121) and VEGF(165) were expressed. In cultured fibroblasts, hypoxia or platelet-derived growth factor (PDGF) raised VEGF production. The angiogenic peptide VEGF is present in all zones of chronic decubital ulcers. Its strong expression within the adjacent granulation tissue supports the view that there is no deficiency of VEGF. VEGF may be involved in the healing process of chronic skin lesions, but it seems that loss of another factor may be responsible for the poor healing response.
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PMID:The angiogenic peptide vascular endothelial growth factor (VEGF) is expressed in chronic sacral pressure ulcers. 1269 51

Cl- channels have been implicated in essential cellular functions including volume regulation, progression of cell cycle, cell proliferation and contraction, but the physiological functions of the ClC-3 channel are controversial. We tested the hypothesis that the ClC-3 gene (ClCn-3) is upregulated in hypertensive pulmonary arteries of monocrotaline-treated rats, and upregulated ClC-3 channel aids viability of pulmonary artery smooth muscle cells (PASMCs). Experimental pulmonary hypertension was induced in rats by a single subcutaneous administration of monocrotaline (60 mg kg(-1)). Injected animals developed characteristic features of pulmonary hypertension including medial hypertrophy of pulmonary arteries and right ventricular hypertrophy. Reverse transcriptase-polymerase chain reaction (RT-PCR), immunohistochemistry and Western immunoblot analysis indicated that histopathological alterations were associated with upregulation of the ClC-3 mRNA and protein expression in both smooth muscle cells of hypertensive pulmonary arteries and in cardiac myocytes. RT-PCR analysis of mRNA, extracted from canine cultured PASMCs, indicated that incubation with the inflammatory mediators endothelin-1 (ET-1), platelet-derived growth factor (PDGF), interleukin-1beta (IL-1beta) and tumor necrosis factor alpha (TNF alpha), but not transforming growth factor beta (TGFbeta), upregulated ClC-3 mRNA. Adenovirus-mediated delivery and overexpression of ClC-3 in canine PASMCs improved cell viability against increasing concentrations of hydrogen peroxide (H2O2, range 50-250 microM). In conclusion, upregulation of ClC-3 in rat hypertensive lung and heart is a novel observation. Our functional data suggest that upregulation of ClC-3 is an adaptive response of inflamed pulmonary artery, which enhances the viability of PASMCs against reactive oxygen species.
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PMID:ClC-3 chloride channel is upregulated by hypertrophy and inflammation in rat and canine pulmonary artery. 1572 95

Fusion of the collagen type I a 1 (COL1A1) gene with the platelet-derived growth factor B-chain (PDGFB) gene has been pointed out in dermatofibrosarcoma protuberans. Various exons of the COL1A1 gene have been shown to be involved in the fusion with exon 2 of the PDGFB gene. We studied the breakpoints of the COL1A1 gene using formalin-fixed, paraffin-embedded tumour specimens from five patients with dermatofibrosarcoma protuberans (three reconfirmations and two new cases). Reverse transcriptase-PCR was performed using paraffin-embedded tissues. Nucleotide sequence analysis was carried out using the PCR products to identify the breakpoints. The COL1A1-PDGFB fusion transcripts were detected from the tumour specimens. Sequence analysis revealed that the ends of exons 18, 29, 38, 42 and 44 in the COL1A1 gene were fused with the start of exon 2 in the PDGFB. This study identified a novel COL1A1 breakpoint, namely, exon 44 of the COL1A1 gene. Detection of the aberrant fusion transcript using formalin-fixed, paraffin-embedded tumour specimens is useful as a diagnostic aid for dermatofibrosarcoma protuberans in cases where fresh or frozen samples of tumour tissue are not available.
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PMID:Gene mutation analysis in five cases of dermatofibrosarcoma protuberans using formalin-fixed, paraffin-embedded tissues. 1604 Apr 6


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