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PMID |
Sentence |
1 |
1353387
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TSP was partially colocalised with the endothelial cell marker, von Willebrand factor, in PDR.
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2 |
16310163
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In this paper, we examined whether Ang II similarly upregulates TSP1 production and TSP1-dependent TGF-beta activation alone or in combination with high glucose concentrations.
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3 |
16310163
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Ang II and high glucose stimulated increases in TSP1 protein levels in the conditioned media of both rat cardiac fibroblasts (RCFs) and rat mesangial cells (RMCs).
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4 |
16310163
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Moreover, Ang II induction of TSP1 and increased TGF-beta activity were blocked by losartan, an antagonist of the Ang II type 1 (AT1) receptor.
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5 |
16310163
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The increase in TSP1 expression leads to increased TGF-beta activity upon Ang II and/or glucose treatment, since peptide antagonists of TSP1-mediated TGF-beta activation blocked Ang II and glucose-induced TGF-beta activation.
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6 |
16630453
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After hemodynamic measurements by the end of the study, myocardial collagen content was quantified in Masson-stained samples and the mRNA expressions of TSP-1 and TGFbeta(1) were detected by quantification real-time RT-PCR.
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7 |
16873687
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In the matrigel, proangiogenic VEGF expression was decreased, while antiangiogenic thrombospondin-1 was upregulated in diabetic mice, regardless of the presence of RAGE.
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8 |
16767790
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Coimmunoprecipitation and radioligand competitive-binding assays confirmed the direct interactions between adiponectin and alpha2M, or TSP-1.
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9 |
17881461
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Our previous studies demonstrated that the transcription factor, upstream stimulatory factor 2 (USF2), was upregulated by high glucose, which bound to an 18-bp sequence in the thrombospondin 1 (TSP1) gene promoter and regulated high glucose-induced TSP1 expression and TGF-beta activity in mesangial cells, suggesting that USF2 might play a role in the development of diabetic nephropathy.
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10 |
19397838
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In response to high glucose, several of these transcription factors regulate the gene encoding the profibrotic cytokine transforming growth factor beta, as well as genes for a range of other proteins implicated in inflammation and extracellular matrix turnover, including thrombospondin 1, the chemokine CCL2, osteopontin, fibronectin, decorin, plasminogen activator inhibitor 1 and aldose reductase.
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11 |
19689798
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Transcription factors PPARgamma, NFAT5, CREB5 and EBF1, the adipokine NAMPT, members of the insulin signaling cascade SORBS1 and IGF1 and IL6ST were repressed, while the adipokine THBS1 and GLUT4 involved in insulin signaling were induced.
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12 |
20689700
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The addition of TSP-1 to primary SMC was sufficient to enhance IGF-I responsiveness in normal glucose.
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13 |
19365032
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We consistently observed lower levels of TSP-1 in diabetic patients who expressed the higher-molecular-weight PEDF isoform.
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14 |
19365032
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Although the PEDF level did not change, the diabetic samples with the higher-molecular-weight PEDF isoform consistently showed lower levels of TSP-1.
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15 |
12644443
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The TSP-1 antagonist LSKL peptide reduced bioactive TGF-beta and fibronectin, indicating the dependence of TGF-beta1 activation on TSP-1.
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16 |
20164378
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It is well established that thrombospondin1 (TSP1) is a major regulator of TGF-beta activation in renal and cardiac complications of diabetes.
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17 |
20164378
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Together, these data establish that glucose-mediated downregulation of PKG levels stimulates TSP1 expression and enhances TGF-beta activity and matrix protein expression, which can contribute to vascular remodeling in diabetes.
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18 |
16816123
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For example, levels of proangiogenic VEGF-A, VEGF-B, neuropilin-1, VEGFR-1, and VEGFR-2 were reduced and the levels of antiangiogenic thrombospondin-1 and retinoblastoma like-2 were increased.
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19 |
20233213
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We have shown that the secreted matrix protein thrombospondin-1 (TSP-1) binds to CD47 and potently inhibits NO stimulation of sGC in endothelial and vascular smooth muscle cells (VSMCs) and platelets.
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20 |
20233213
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Here we show that TSP-1 signalling via CD47 inhibits sGC activation by NO-independent sGC activating small molecules.
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21 |
20233213
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TSP-1 pretreatment also inhibited the ability of these agents to delay thrombin-induced platelet aggregation.
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22 |
18515748
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The constitutively active form of AhR induced activation of the thrombospondin-1 gene promoter.
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