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Am J Physiol Renal Physiol 280: F657-F666, 2001;
0363-6127/01 $5.00
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Vol. 280, Issue 4, F657-F666, April 2001

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

Charles W. Heilig1,2,3, Jeffrey I. Kreisberg4, Svend Freytag3, Takashi Murakami5, Yousuke Ebina5, Lirong Guo2, Kathleen Heilig1,2, Robert Loberg6, Xuan Qu6, Ying Jin1, Douglas Henry7, and Frank C. Brosius III6

1 Division of Nephrology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205; 2 Nephrology Unit, University of Rochester Medical Center, Rochester, New York 14642; 3 Division of Molecular Biology, Henry Ford Hospital, Detroit 48202; 6 Division of Nephrology, Department of Medicine and Veterans Affairs Medical Center, University of Michigan, Ann Arbor 48109; 7 Department of Physiology, College of Human Medicine, Michigan State University, East Lansing, Michigan 48824; 4 Department of Surgery, University of Texas Health Science Center and the Audie Murphy Veterans Administration Hospital, San Antonio, Texas 78284; and 5 School of Medicine, Tokushima University, Tokushima 770, Japan

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-[3H]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.

glucose; GLUT-1; antisense; chloramphenicol acetyltransferase assay; fibronectin


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