Vascular permeability factor mRNA and protein expression in human kidney

Brown, Lawrence F.; Berse, Brygida; Tognazzi, Kathi; Manseau, Eleanor J.; Water, Livingston Van De; Senger, Donald R.; Dvorak, Harold F.; Rosen, Seymour

doi:10.1038/ki.1992.441

Cited by 263 publications

(171 citation statements)

References 22 publications

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“…3). This is in agreement with an earlier report showing that Flt-1 and Flk-1 are expressed at low levels in endothelial cells under normal conditions, but are up-regulated at sites where there is a concomitant up-regulation of VEGF (45). Activation of Flt-1 by VEGF does not efficiently induce migration of endothelial cells without simultaneous Flk/KDR activation (46).…”

Section: Discussionsupporting

confidence: 81%

Vascular Endothelial Growth Factor Expression and Regulation of Murine Collagen-Induced Arthritis

Kasama

Kobayashi

et al. 2000

The Journal of Immunology

130

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We have examined the expression and function of the angiogenic factor, vascular endothelial growth factor (VEGF) during the evolution of type II collagen-induced arthritis (CIA). Biologically active VEGF was expressed along a time course that paralleled the expression of two specific VEGF receptors, Flk-1 and Flt-1, and the progression of joint disease. Moreover, levels of VEGF expression correlated with the degree of neovascularization, as defined by vWF levels, and arthritis severity. Macrophage- and fibroblast-like cells, which infiltrated inflamed sites and were then activated by other inflammatory mediators, are probably important sources of VEGF and may thus regulate angiogenesis during the development of CIA. Administration of anti-VEGF antiserum to CIA mice before the onset of arthritis delayed the onset, reduced the severity, and diminished the vWF content of arthritic joints. By contrast, administration of anti-VEGF antiserum after the onset of the disease had no effect on the progression or ultimate severity of the arthritis. These data suggest that VEGF plays a crucial role during an early stage of arthritis development, affecting both neovascularization and the progression of experimentally induced synovitis.

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Section: Discussionsupporting

confidence: 81%

Vascular Endothelial Growth Factor Expression and Regulation of Murine Collagen-Induced Arthritis

Kasama

Kobayashi

et al. 2000

The Journal of Immunology

130

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“…So far VEGF expression in normal human and rat kidney has been known to be confined to podocytes and distal and collecting duct epithelium (10,18). GEC have been identified as the site of constitutive production of VEGF (19). Formation of fenestrae and increased permeability of glomerular endothelial cells have been attributed to VEGF produced by GEC (7), facilitating the high rate of glomerular filtration.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, nephrin mRNA was detected in GEC. A monoclonal antibody GSA3 recognizing a cell-specific surface antigen on podocytes (19) showed positive immunostaining of GEC. Furthermore, puromycin exerted cytotoxic effect in GEC, and cells lacked markers characteristic of endothelial and mesangial cells-von Willebrand factor and Thy-1 antigen (not shown).…”

Section: Cell Culturesmentioning

confidence: 99%

VEGF Expression in Hypoxia and Hyperglycemia

Kim

Chen

Weinstein

et al. 2002

Journal of the American Society of Nephrology

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ABSTRACT. Vascular endothelial growth factor (VEGF), an angiogenic factor for endothelial cells, is produced by glomerular and tubular epithelia. Using immunoelectron microscopy, VEGF expression by podocytes (GEC) and the proximal tubular epithelium of rat kidney was confirmed. To elucidate the mechanisms of VEGF production and its physiologic consequences, studies were performed in cultured GEC and proximal tubular epithelial cells (RPTEC). Both GEC and RPTEC expressed VEGF-120 and 164 mRNA, as detected by quantitative RT-PCR. Hypoxia resulted in an increase in mRNA abundance, more robust in RPTEC than in GEC, and an increase in VEGF expression by 1.9- and 1.6-fold, respectively. 30 mM d-glucose, but not 30 mM l-glucose, resulted in the elevation of VEGF mRNA in RPTEC, but not in GEC, although both cell types showed a comparable modest increase in VEGF expression. Combined treatment (hypoxia and 30 mM d-glucose) resulted in an increase of VEGF mRNA only in RPTEC; however, an enhanced protein expression was detectable in both cell types. To investigate the role of VEGF in branching angiogenesis, “sandwich” co-cultures were applied with endothelial cells and capillary tube formation was compared under the above conditions. Both RPTEC and GEC induced VEGF-dependent capillary tube formation by co-cultured endothelial cells and in both cell types hypoxia further augmented angiogenesis. In contrast, 30 mM d-glucose suppressed angiogenesis in co-cultures with both cell types despite increased mRNA for VEGF receptors 1 and 2. This study shows (1) that VEGF produced by GEC and RPTEC is necessary for branching angiogenesis and (2) that hypoxic environment stimulates VEGF production by both epithelial cell types and augments branching angiogenesis, whereas (3) hyperglycemic microenvironment, although also stimulatory for VEGF production, fails to augment angiogenesis.

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“…It is expressed at low concentrations in a wide variety of normal adult human and animal tissues and at higher concentrations in a few select sites, namely podocytes of the renal glomeruli and cardiac myocytes [38,39]. Human mesangial cells and peripheral blood mononuclear cells produce VEGF in vitro [40].…”

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confidence: 99%