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

Chaeles W. Heilig, Jeffrey I. Kreisberg, Svend Freytag, Takashi Murakami, Yousuke Ebina, Lirong Guo, Kathleen Heilig, Robert Loberg, Xuan Qu, Ying Jin, Douglas Henry, Frank C. Brosius

Resultado de la investigación: Articlerevisión exhaustiva

46 Citas (Scopus)


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.

Idioma originalEnglish (US)
Páginas (desde-hasta)F657-F666
PublicaciónAmerican Journal of Physiology - Renal Physiology
N.º4 49-4
EstadoPublished - abr 2001
Publicado de forma externa

ASJC Scopus subject areas

  • Physiology
  • Urology


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