Redistribution of cytoplasmic VEGF to the basolateral aspect of renal tubular cells in ischemia-reperfusion injury

Kanellis, John; Mudge, Stuart J.; Fraser, Scott A; Katerelos, Marina; Power, David A.

doi:10.1046/j.1523-1755.2000.00103.x

Cited by 54 publications

(55 citation statements)

References 43 publications

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“…However, human cell lines were demonstrated recently to present decreased expression levels of HO-1 under hypoxia, with protein Bach-1 being implicated as a hypoxia-inducible repressor for the HO-1 gene (25). In addition, a peculiar response to experimental hypoxia has been demonstrated in the kidney, which may redistribute the pre-existing VEGF protein, rather than increase mRNA and protein synthesis (26).…”

Section: Discussionmentioning

confidence: 99%

Differential Expression of Heme Oxygenase-1 and Vascular Endothelial Growth Factor in Cadaveric and Living Donor Kidneys after Ischemia-Reperfusion

Lemos

IJzermans²,

Zondervan³

et al. 2003

Journal of the American Society of Nephrology

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Abstract. The extent of graft damage after ischemia-reperfusion reflects the balance between deleterious events and protective factors. Heme oxygenase-1 (HO-1) and vascular endothelial growth factor (VEGF) may contribute to cytoprotection by their anti-inflammatory and antiapoptotic properties. For investigating whether HO-1 and VEGF play a role in the adaptive response to ischemia-reperfusion injury after renal transplantation, kidney biopsies were analyzed from living (n ϭ 45) and cadaveric (n ϭ 16) donors, obtained at three time points: at the end of cold storage T(Ϫ1), after warm ischemia T(0), and after reperfusion T(ϩ1). The mRNA expression levels of HO-1, VEGF 165 , Bcl-2, Bax, and hypoxia inducible factor-1␣ were quantified by real-time reverse transcriptase-PCR, and the HO-1 and VEGF proteins were analyzed by immunohistochemistry. Cadaveric donor kidneys presented higher mRNA expression levels of hypoxia inducible factor-

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Section: Discussionmentioning

confidence: 99%

Differential Expression of Heme Oxygenase-1 and Vascular Endothelial Growth Factor in Cadaveric and Living Donor Kidneys after Ischemia-Reperfusion

Lemos

IJzermans²,

Zondervan³

et al. 2003

Journal of the American Society of Nephrology

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“…In the rat, normal kidney showed diffuse expression of VEGF in all tubules of the renal cortex and medulla (20). However, proximal tubules in the human kidney exhibit only faint, if any, labeling of VEGF mRNA and VEGF protein when studied by in situ hybridization and immunohistochemistry (19,20,21).…”

Section: Discussionmentioning

confidence: 99%

“…However, proximal tubules in the human kidney exhibit only faint, if any, labeling of VEGF mRNA and VEGF protein when studied by in situ hybridization and immunohistochemistry (19,20,21). Only one publication reported that human proximal tubular cells produced VEGF in culture (22).…”

Section: Discussionmentioning

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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“…However, the specific signaling pathway and downstream target genes activated by Etk are still elusive. Since VEGF has been shown to be a survival factor for epithelial cells (Kanellis et al, 2000) and is also upregulated by hypoxia (Jiang et al, 2000), we examined herein whether VEGF could be an Etk downstream target gene and whether Etk is involved in the signaling cascade that leads to the activation of VEGF expression in both normoxia and hypoxia conditions. Hence, Northern blot analyses were performed on total RNAs prepared from Pa-4 and Pa-4DEtk : ER cells.…”

Section: Induction Of Vegf Expression By Etk Activation In Pa-4detk :mentioning

confidence: 99%

“…Moreover, VEGF was found to stimulate DNA synthesis of endothelial cells preferentially through the same receptor, activating a distinct ERK1/2 pathway (Kanno et al, 2000), which was considered indispensable for the survival of endothelial cells (Gupta et al, 1999). Furthermore, these observations have recently been extended to renal tubular epithelial cells, suggesting that VEGF also promotes the survival of certain epithelial cells (Kanellis et al, 2000). Consequently, alterations in the expression and activity of VEGF have been postulated to play a crucial role in acquisition of the migrating and invasive tumorigenic properties of human malignant cells (Bagheri-Yarmand et al, 2001).…”

Section: Introductionmentioning

confidence: 95%

Coordinating Etk/Bmx activation and VEGF upregulation to promote cell survival and proliferation

et al. 2002

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Redistribution of cytoplasmic VEGF to the basolateral aspect of renal tubular cells in ischemia-reperfusion injury

Cited by 54 publications

References 43 publications

Differential Expression of Heme Oxygenase-1 and Vascular Endothelial Growth Factor in Cadaveric and Living Donor Kidneys after Ischemia-Reperfusion

Differential Expression of Heme Oxygenase-1 and Vascular Endothelial Growth Factor in Cadaveric and Living Donor Kidneys after Ischemia-Reperfusion

VEGF Expression in Hypoxia and Hyperglycemia

Coordinating Etk/Bmx activation and VEGF upregulation to promote cell survival and proliferation

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