Vascular endothelial growth factor induces manganese‐superoxide dismutase expression in endothelial cells by a Racl‐regulated NADPH oxidase‐dependent mechanism

Abid, M. Ruhul; Tsai, Jo C.; Spokes, Katherine; Deshpande, Shailesh; Irani, Kaikobad; Aird, William C.

doi:10.1096/fj.01-0338fje

Cited by 155 publications

(119 citation statements)

References 72 publications

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“…It has been demonstrated that small amounts of ROS are produced after cell stimulation with a variety of hormones and growth factors, including VEGF, following binding to cell membrane receptors [43]. Low concentrations of ROS may even mimic the action of growth factors [44].…”

Section: Discussionmentioning

confidence: 99%

Psoriasin (S100A7) increases the expression of ROS and VEGF and acts through RAGE to promote endothelial cell proliferation

Shubbar

Vegfors

Carlström

et al. 2011

Breast Cancer Res Treat

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Psoriasin (S100A7), originally identified in psoriasis, is a calcium-binding protein belonging to the multigenic S100 family. In high-grade ductal carcinoma in situ (DCIS), psoriasin was identified as one of the most abundant transcripts. We have previously shown that psoriasin was induced by reactive oxygen species (ROS). Moreover, the downregulation of psoriasin by short hairpin RNA (shRNA) led to the reduced expression of VEGF and inhibited tumour Our data suggest that psoriasin expression in mammary epithelial cells leads to increased endothelial cell proliferation in a paracrine manner through RAGE. Psoriasin may therefore play a role in breast cancer progression by promoting oxidative stress response and angiogenesis.

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Section: Discussionmentioning

confidence: 99%

Psoriasin (S100A7) increases the expression of ROS and VEGF and acts through RAGE to promote endothelial cell proliferation

Shubbar

Vegfors

Carlström

et al. 2011

Breast Cancer Res Treat

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“…Western and Northern Blot Analyses-Immunoblot assays were performed by modification of the procedure previously described (55). Briefly, CASMC were washed in phosphate-buffered saline twice and harvested by scraping in 20 mM Tris-HCl (pH 7.5), 150 mM NaCl, 1 mM EDTA, 1 mM EGTA, 1% Triton X-100, 20 mM ␤-glycerophosphate, 10 mM sodium pyrophosphate, 10 mM sodium vanadate, 1 g/ml leupeptin, 1 mM NaF, and 1 mM phenylmethylsulfonyl fluoride, and protease inhibitor mixture (Roche Applied Science).…”

Section: Methodsmentioning

confidence: 99%

Forkhead Transcription Factors Inhibit Vascular Smooth Muscle Cell Proliferation and Neointimal Hyperplasia

Abid

Yano

Guo

et al. 2005

Journal of Biological Chemistry

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113

107

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Vascular smooth muscle cell (VSMC) proliferation and migration contribute significantly to atherosclerosis, postangioplasty restenosis, and transplant vasculopathy. Forkhead transcription factors belonging to the FoxO subfamily have been shown to inhibit growth and cell cycle progression in a variety of cell types. We hypothesized that forkhead proteins may play a role in VSMC biology. Under in vitro conditions, platelet-derived growth factor (PDGF)-BB, tumor necrosis factor-␣, and insulin-like growth factor 1 stimulated phosphorylation of FoxO in human coronary artery smooth muscle cells via MEK1/2 and/or phosphatidylinositol 3-kinasedependent signaling pathways. PDGF-BB, tumor necrosis factor-␣, and insulin-like growth factor 1 treatment resulted in the nuclear exclusion of FoxO, whereas PDGF-BB alone down-regulated the FoxO target gene, p27 kip1 , and enhanced cell survival and progression through the cell cycle. These effects were abrogated by overexpression of a constitutively active, phosphorylation-resistant mutant of the FoxO family member, TM-FKHRL1. The anti-proliferative effect of TM-FKHRL1 was partially reversed by small interfering RNA against p27 kip1 . In a rat balloon carotid arterial injury model, adenovirus-mediated gene transfer of FKHRL1 caused an increase in the expression of p27 kip1 in the VSMC and inhibition of neointimal hyperplasia. These data suggest that FoxO activity inhibits VSMC proliferation and activation and that this signaling axis may represent a therapeutic target in vasculopathic disease states.

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“…The signals were quantified with Image (National Institutes of Health), and statistical analyses were carried out using the Student t test. Cell migration assays were carried out by modified Boyden chamber, as previously described (20).…”

Section: Methodsmentioning

confidence: 99%

Thrombin Stimulation of Vascular Adhesion Molecule-1 in Endothelial Cells Is Mediated by Protein Kinase C (PKC)-δ-NF-κB and PKC-ζ-GATA Signaling Pathways

Minami

Abid

Zhang

et al. 2003

Journal of Biological Chemistry

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106

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We recently demonstrated that thrombin induces the expression of vascular adhesion molecule-1 (VCAM-1) in endothelial cells by an NF-B-and GATA-dependent mechanism. In the present study, we describe the signaling pathways that mediate this response. Thrombin stimulation of the VCAM-1 gene and promoter in human umbilical vein endothelial cells was inhibited by preincubation with the phosphatidylinositol 3-kinase inhibitor, LY294002, the protein kinase C (PKC)-␦ inhibitor, rottlerin, a PKC-peptide inhibitor, or by overexpression of dominant negative (DN)-PKC-. In electrophoretic mobility shift assays, thrombin-mediated induction of NF-B p65 binding to two NF-B motifs in the upstream promoter region of VCAM-1 was blocked by LY294002 and rottlerin, whereas the inducible binding of GATA-2 to a tandem GATA motif was inhibited by LY294002 and the PKC-peptide inhibitor. In co-transfection assays, thrombin stimulation of a minimal promoter containing multimerized VCAM-1 NF-B sites was inhibited by DN-PKC-␦ but not DN-PKC-. In contrast, thrombin-mediated transactivation of a minimal promoter containing tandem VCAM-1 GATA motifs was inhibited by DN-PKC-but not DN-PKC-␦. Finally, thrombin failed to induce VCAM-1 expression in vascular smooth muscle cells. Taken together, these data suggest that the endothelial cell-specific effect of thrombin on VCAM-1 expression involves the coordinate activity of PKC-␦-NF-B and PKC--GATA signaling pathways. Vascular adhesion molecule-1 (VCAM-1)1 is a 110-kDa cell surface glycoprotein that is expressed in cytokine-activated endothelial cells (1). The VCAM-1 promoter, originally cloned and characterized in cultured endothelial cells (2), represents a potentially valuable tool for dissecting the molecular mechanisms of endothelial cell activation. Several studies have demonstrated the importance of two tandem NF-B elements located at position Ϫ77 and Ϫ63, relative to the transcriptional start site, in transducing the response to inflammatory mediators (2-4). Other studies have provided evidence for the role of co-stimulators in mediating cytokine response, including Sp1 (5), activating protein-1 (6), and interferon regulatory factor-1 (7).In a recent report, we showed that the incubation of endothelial cells with thrombin or the PAR-1 agonist, thrombin receptor activation peptide (TRAP), resulted in increased VCAM-1 mRNA levels and VCAM-1 promoter activity (8). Not surprisingly, a mutation of the tandem NF-B motif blocked the response to thrombin. Moreover, in electrophoretic mobility shift assays, thrombin induced the binding of p65 homodimers to the two adjacent NF-B sites in the VCAM-1 promoter. A more interesting finding was that a mutation of a tandem GATA motif (located at Ϫ244 and Ϫ259) also attenuated the thrombin response. Consistent with these results, thrombin treatment resulted in increased binding of GATA-2 to the VCAM-1 promoter. These data suggested that thrombin-mediated induction of VCAM-1 involves the coordinate activity of NF-B p65 and GATA-2 and raised new questions as to...

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Vascular endothelial growth factor induces manganese‐superoxide dismutase expression in endothelial cells by a Racl‐regulated NADPH oxidase‐dependent mechanism

Cited by 155 publications

References 72 publications

Psoriasin (S100A7) increases the expression of ROS and VEGF and acts through RAGE to promote endothelial cell proliferation

Psoriasin (S100A7) increases the expression of ROS and VEGF and acts through RAGE to promote endothelial cell proliferation

Forkhead Transcription Factors Inhibit Vascular Smooth Muscle Cell Proliferation and Neointimal Hyperplasia

Thrombin Stimulation of Vascular Adhesion Molecule-1 in Endothelial Cells Is Mediated by Protein Kinase C (PKC)-δ-NF-κB and PKC-ζ-GATA Signaling Pathways

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