Antisense GLUT-1 protects mesangial cells from glucose induction of GLUT-1 and fibronectin expression.

Heilig CW; Kreisberg JI; Freytag S; Murakami T; Ebina Y; Guo L; Heilig K; Loberg R; Qu X; Jin Y; Henry D; Brosius FC 3rd

doi:10.1152/ajprenal.2001.280.4.f657

Antisense GLUT-1 protects mesangial cells from glucose induction of GLUT-1 and fibronectin expression.

Guo L ,

Qu X ,

Jin Y ,

Henry D ,

Brosius FC 3rd

Affiliations

1. Division of Nephrology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
Authors
Heilig CW¹
(1 author)

American Journal of physiology. Renal Physiology, 01 Apr 2001, 280(4):F657-66
https://doi.org/10.1152/ajprenal.2001.280.4.f657 PMID: 11249857

Abstract

A stable clone of rat mesangial cells expressing antisense GLUT-1 (i.e., MCGT1AS cells) was developed to protect them from high glucose exposure. GLUT-1 protein was reduced 50%, and the 2-deoxy-[(3)H]glucose uptake rate was reduced 33% in MCGT1AS. MCLacZ control cells and MCGT1 GLUT-1-overexpressing cells were used for comparisons. In MCLacZ, 20 mM D-glucose increased GLUT-1 transcription 90% vs. no increase in MCGT1AS. Glucose (8 mM) and 12 mM xylitol [a hexose monophosphate (HMP) shunt substrate] did not stimulate GLUT-1 transcription. An 87% replacement of the standard 8 mM D-glucose with 3-O-methylglucose reduced GLUT-1 transcription 80%. D-Glucose (20 mM) increased fibronectin mRNA and protein by 47 and 100%, respectively, in MCLacZ vs. no increases in MCGT1AS. Fibronectin synthesis was elevated 48% in MCGT1 and reduced 44% in MCGT1AS. We conclude that 1) transcription of GLUT-1 in response to D-glucose depends on glucose metabolism, although not through the HMP shunt, and 2) antisense GLUT-1 treatment of mesangial cells blocks D-glucose-induced GLUT-1 and fibronectin expression, thereby demonstrating a protective effect that could be beneficial in the setting of diabetes.

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NIDDK NIH HHS (3)

Grant ID: 1 RO1 DK-54507-01
1 publication
Grant ID: 1-K08-DK-01953
1 publication
Grant ID: K11-DK-02193
2 publications

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Antisense GLUT-1 protects mesangial cells from glucose induction of GLUT-1 and fibronectin expression.

Affiliations

Authors

Abstract

Full text links

References

High glucose causes an increase in extracellular matrix proteins in cultured mesangial cells.

Title not supplied

Polyol pathway mediates high glucose-induced collagen synthesis in proximal tubule.

Prevention of diabetic nephropathy in db/db mice with glycated albumin antagonists. A novel treatment strategy.

Activation of protein kinase C in glomerular cells in diabetes. Mechanisms and potential links to the pathogenesis of diabetic glomerulopathy.

The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus.

Effects of hyperglycemia on glucose transporters of the muscle: use of the renal glucose reabsorption inhibitor phlorizin to control glycemia.

Receptor-specific increase in extracellular matrix production in mouse mesangial cells by advanced glycosylation end products is mediated via platelet-derived growth factor.

Title not supplied

Abnormalities in protein kinase C and MAP kinase cascade in mesangial cells cultured under high glucose conditions.

Citations & impact

Impact metrics

Citations of article over time

Article citations

Inhibition of eIF5A hypusination reprogrammes metabolism and glucose handling in mouse kidney.

Anthocyanins as Antidiabetic Agents-In Vitro and In Silico Approaches of Preventive and Therapeutic Effects.

The contribution of genetic variants of SLC2A1 gene in T2DM and T2DM-nephropathy: association study and meta-analysis.

Changes in glucose transporter expression and nitric oxide production are associated with liver injury in diabetes.

Podocytes and the struggle against glucose toxicity: new targets for treatment?

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