The regulation of the induction of vascular endothelial growth factor at the onset of diabetes in spontaneously diabetic rats

Braun, László; Kardon, Tamás; Zs, Reisz-Porszasz; Bánhegyi, Gábor; Mandl, József

doi:10.1016/s0024-3205(01)01327-3

Cited by 34 publications

(27 citation statements)

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“…These findings agree with those of a previous report that found that renal VEGF mRNA expression increases during the early period of diabetic nephropathy in type II diabetic rats (Tsuchida et al 1999, Braun et al 2001, Hoshi et al 2002). An early and persistent increase in renal VEGF gene expression was also described in streptozotocininduced diabetic rats (Cooper et al 1999).…”

Section: Discussionsupporting

confidence: 93%

Vascular endothelial growth factor is increased during early stage of diabetic nephropathy in type II diabetic rats

Ryong

Kang²,

Han

et al. 2004

Journal of Endocrinology

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Vascular endothelial growth factor (VEGF) has been implicated in the pathogenesis of diabetic nephropathy. We investigated serial changes of VEGF in the kidney and assessed whether glomerular and urinary VEGF levels are related to the severity of diabetic nephropathy. Furthermore, we examined the relationship between urinary VEGF levels and the urinary albumin excretion (UAE) rate in Otsuka-Long-Evans-Tokushima-Fatty (OLETF) rats. Glomerular VEGF mRNA expression and protein synthesis were evaluated by the reverse transcriptionpolymerase chain reaction, immunohistochemical staining and in situ hybridization. Urinary levels of VEGF were determined by enzyme-linked immunosorbent assay. UAE was significantly higher in OLETF rats than in control Long-Evans-Tokushima-Fatty (LETO) rats throughout the study period. Urinary VEGF levels were significantly higher from 25 to 37 weeks, and then gradually reduced until 55 weeks, although the levels were still higher than those in control rats. Urinary VEGF levels also showed a significant positive correlation with UAE (r=0·262, P=0·045) and serum creatinine (r=0·398, P=0·044), and were found to be independently correlated with UAE by Spearman's rank correlation. By immunohistochemical staining and in situ hybridization, VEGF was mainly detected in the podocytes in the glomeruli. Interestingly, a significant increase in VEGF mRNA expression was observed in the early period of diabetic nephropathy, and this was associated with increased urinary VEGF excretion. Thus, the overproduction of VEGF in the diabetic kidney may participate in the pathogenesis of early-stage diabetic nephropathy.

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Section: Discussionsupporting

confidence: 93%

Vascular endothelial growth factor is increased during early stage of diabetic nephropathy in type II diabetic rats

Ryong

Kang²,

Han

et al. 2004

Journal of Endocrinology

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“…Braun et al (2001) reported that the hypoxia responsive element and CRE are equally involved in the regulation of VEGF expression in various tissues in diabetic rats.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin II stimulates the synthesis of vascular endothelial growth factor through the p38 mitogen activated protein kinase pathway in cultured mouse podocytes

Kang¹,

Park²,

Kim³

et al. 2006

Journal of Molecular Endocrinology

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“…A number of studies have demonstrated crossspecificity between HIF-1 and CREB at the level of binding to HRE and CRE sequences (4,11,21,22). Specifically, CREB has been shown to have binding affinity for the HRE sequence and may be of importance in the hypoxic upregulation of genes such as lactate dehydrogenase.…”

Section: Discussionmentioning

confidence: 99%

Hypoxia induces epithelial amphiregulin gene expression in a CREB-dependent manner

O’Reilly

Leonard²,

Kieran³

et al. 2006

American Journal of Physiology-Cell Physiology

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Hypoxia occurs during a number of conditions in which altered epithelial proliferation is critical, including tumor development. Microarray analysis of colon-derived epithelial cells revealed a hypoxia-dependent increase in the expression of amphiregulin, an EGF receptor (EGFR) ligand that activates epithelial proliferation and has been associated with the development of colonic tumors. Amphiregulin expression was also induced in tissues from mice exposed to whole animal hypoxia. The hypoxic upregulation of amphiregulin was independent of the classic transcriptional response mediated via hypoxia-inducible factor (HIF)-1α. Transfection of HeLa cells with truncated amphiregulin promoter reporter constructs revealed that a 37-bp segment upstream from the TATA box retained hypoxic sensitivity. This sequence contains an evolutionarily conserved cAMP response element (CRE) that constitutively binds the CRE binding protein (CREB). Deletion of the CRE abolished sensitivity to hypoxia. Thus hypoxia promotes intestinal epithelial amphiregulin expression in a CRE-dependent manner, an event that may contribute to increased proliferation. These data also further support a role for CREB as an HIF-independent hypoxia-responsive transcription factor in the regulation of intestinal epithelial gene expression.

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The regulation of the induction of vascular endothelial growth factor at the onset of diabetes in spontaneously diabetic rats

Cited by 34 publications

References 0 publications

Vascular endothelial growth factor is increased during early stage of diabetic nephropathy in type II diabetic rats

Vascular endothelial growth factor is increased during early stage of diabetic nephropathy in type II diabetic rats

Angiotensin II stimulates the synthesis of vascular endothelial growth factor through the p38 mitogen activated protein kinase pathway in cultured mouse podocytes

Hypoxia induces epithelial amphiregulin gene expression in a CREB-dependent manner

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