Angiogenesis and G-protein-coupled receptors: signals that bridge the gap

Richard, Darren E.; Vouret‐Craviari, Valérie; Pouysségur, Jacques

doi:10.1038/sj.onc.1204193

Cited by 91 publications

(79 citation statements)

References 74 publications

(66 reference statements)

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“…Interestingly, the G-protein beta 3 subunit gene (GNB3) is located very near to the VDR locus (12q12-q13 and 12q12-q14, respectively), and this family of proteins has been associated with many regulatory functions including cell growth and angiogenesis [53]. One report has showed an association between diabetic nephropathy and a genetic variant in the G-protein beta 3 subunit, C825T polymorphism [54].…”

Section: Discussionmentioning

confidence: 99%

Taq I polymorphism of the vitamin D receptor and risk of severe diabetic retinopathy

et al. 2002

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Neovascularization plays a role in determining the severity of diabetic retinopathy (DR) due to the effects of several angiogenic and growth factors, including vascular endothelial growth factor (VEGF), plateletderived growth factor (PDGF), basic fibroblast growth factor (bFGF) and insulin-like growth factor (IGF-1) [1].Chronic hyperglycaemia induces non-severe diabetic retinopathy (DR) in most patients of long duration, but not severe DR in the majority of them, sug- Abstract Aims/hypothesis. Vitamin D, a molecule with antiproliferative, antiangiogenic, antioxidant and immunosuppressive effects, could play a role in the pathogenesis of severe diabetic retinopathy. We examined whether Taq I polymorphism of the vitamin D receptor is involved in the development of severe diabetic retinopathy. Methods. 200 unrelated C-peptide-negative French Type I diabetic patients were randomly selected (male:female, 103:97, age 44.4 12.4 years, diabetes duration: 27.7 10.0 years, BMI: 24.3 3.4 kg/m 2 , HbA 1 c : 8.6 1.3 %). The Taq I site was analysed by PCR followed by digestion with Taq I enzyme. Diabetic retinopathy was assessed by retinal angiography and classified as presence (n = 101) or absence (n = 99) of severe (preproliferative or proliferative) diabetic retinopathy. Results. Frequency of wild-type genotype TT was lower in patients with severe diabetic retinopathy (n = 27) when compared with control subjects (n = 42, OR = 0.5, p = 0.028). Allele frequencies were not different between patients (T: n = 112 and t: n = 90) and control subjects (T: n = 128, and t: n = 70, p = 0.075). Global c 2 (df = 2): p = 0.064. In subjects with diabetes duration of more than 25 years, TT was lower in severe diabetic retinopathy (n = 14) than control subjects (n = 18, OR = 0.3, p = 0.01). Allele frequencies were different between patients (T: n = 68 and t: n = 66) and control subjects (T: n = 52, OR = 0.5, and t: n = 26, OR = 1.9, p = 0.034). Global c 2 (df = 2): p = 0.024. In subjects with HbA 1 c over 9 %, Tt was higher in patients (n = 28) than control subjects (n = 15, OR = 3.1, p = 0.019). Allele frequencies were not different between patients (T: n = 52 and t: n = 38) and control subjects (T: n = 57, and t: n = 29, p = 0.31). Global c 2 (df = 2): p = 0.035. Conclusion/interpretation. In French Type I (insulindependent) diabetic patients, we demonstrate an association between TT form (VDR) and low risk for severe diabetic retinopathy, especially in patients with long duration, and between Tt variant and high risk for severe diabetic retinopathy in subjects with poor glycaemic control. [Diabetologia (2002) 45: 436±442]

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Section: Discussionmentioning

confidence: 99%

Taq I polymorphism of the vitamin D receptor and risk of severe diabetic retinopathy

et al. 2002

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“…Vascular endothelial growth factor is known to be the main angiogenic factor in ovarian cancer (Yamamoto et al, 1997;Fujimoto et al, 1998;Bamberger and Perrett, 2002). It has been shown that angiotensin II upregulated VEGF expression via AT 1 R (Chua et al, 1998;Pupilli et al, 1999;Tamarat et al, 2002), and this angiotensin II-induced VEGF upregulation was mediated by hypoxia-inducible factor-1, even in non-hypoxic conditions (Richard et al, 2001). We have recently reported that angiotensin II stimulated VEGF expression and secretion in AT 1 R-positive ovarian cancer cells in vitro (Suganuma et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Angiotensin II type 1 receptor expression in ovarian cancer and its correlation with tumour angiogenesis and patient survival

et al. 2006

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Angiotensin II, a main effector peptide in the renin -angiotensin system, acts as a growth-promoting and angiogenic factor via type 1 angiotensin II receptors (AT 1 R). We have recently demonstrated that angiotensin II enhanced tumour cell invasion and vascular endothelial growth factor (VEGF) secretion via AT 1 R in ovarian cancer cell lines in vitro. The aim of the present study was to determine whether AT 1 R expression in ovarian cancer is correlated with clinicopathological parameters, angiogenic factors and patient survival. Immunohistochemical staining for AT 1 R, VEGF, CD34 and proliferating cell nuclear antigen (PCNA) were analysed in ovarian cancer tissues (n ¼ 67). Intratumour microvessel density (MVD) was analysed by counting the CD34-positive endothelial cells. Type 1 angiotensin II receptors were expressed in 85% of the cases examined, of which 55% were strongly positive. Type 1 angiotensin II receptors expression was positively correlated with VEGF expression intensity and MVD, but not with histological subtype, grade, FIGO stage or PCNA labelling index. In patients who had positive staining for AT 1 R, the overall survival and progression-free survival were significantly poor (P ¼ 0.041 and 0.017, respectively) as compared to those in patients who had negative staining for AT 1 R, although VEGF, but not AT 1 R, was an independent prognostic factor on multivariate analysis. These results demonstrated that AT 1 R correlated with tumour angiogenesis and poor patient outcome in ovarian cancer, suggesting its clinical potential for a novel molecular target in strategies for ovarian cancer treatment.

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“…For example, it was shown that activation of G-protein-coupled receptor (36) results in HIF-1␣ induction, most likely by activity of GTPase Rac1 (60). This pathway may lead to stabilization of HIF-1␣ by the production of reactive oxygen species (61). It would be interesting to test in future studies whether the TCR-triggered biochemical pathway is able to affect the HIF-1␣-pVHL interactions.…”

Section: Discussionmentioning

confidence: 99%

Differential Regulation of Two Alternatively Spliced Isoforms of Hypoxia-inducible Factor-1α in Activated T Lymphocytes

Lukashev

Caldwell

Ohta

et al. 2001

Journal of Biological Chemistry

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Cell adaptation to hypoxia is partially accomplished by hypoxia-inducible transcription factor-1 (HIF-1).Here we report the hypoxia-independent up-regulation of HIF-1␣ subunit in antigen receptor-activated T cells. This is explained by a selective up-regulation of alternatively spliced mRNA isoform I.1 that encodes the HIF-1␣ protein without the first 12 N-terminal amino acids. We show that both short (I.1) and long (I.2) HIF-1␣ isoforms display similar DNA binding and transcriptional activities. Major differences were observed between these two HIF-1␣ isoforms in their expression patterns with respect to the resting and activated T lymphocytes in hypoxic and normoxic conditions. The T cell antigen receptor (

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Angiogenesis and G-protein-coupled receptors: signals that bridge the gap

Cited by 91 publications

References 74 publications

Taq I polymorphism of the vitamin D receptor and risk of severe diabetic retinopathy

Taq I polymorphism of the vitamin D receptor and risk of severe diabetic retinopathy

Angiotensin II type 1 receptor expression in ovarian cancer and its correlation with tumour angiogenesis and patient survival

Differential Regulation of Two Alternatively Spliced Isoforms of Hypoxia-inducible Factor-1α in Activated T Lymphocytes

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