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II in neonatal mesangial cells
1 Division of Nephrology, Department of Medicine, Case Western Reserve University and University Hospitals of Cleveland, Cleveland 44106; and 2 Division of Nephrology, Department of Medicine, Case Western Reserve University and the Cleveland Veteran's Administration Medical Center, Cleveland, Ohio 44106
Increased activation of specific protein kinase C (PKC)
isoforms and increased nonenzymatic glycation of intracellular and extracellular proteins [the accumulation of advanced glycation end products (AGEs)] are major mechanistic pathways implicated in
the pathogenesis of diabetic complications. Blocking
PKC-
II has been shown to decrease albuminuria in animal
models of diabetes. To demonstrate a direct relationship between AGEs
and the induction and translocation of PKC-II, studies
were carried out in rat neonatal mesangial cells, known to express
PKC-II in association with rapid proliferation in
post-natal development. Oxidative stress was studied by using the
fluorescent probe dichlorfluorescein diacetate. Translocation of
PKC-II was demonstrated by using immunofluorescence and
Western blotting of fractionated mesangial cells. Induction of
intracellular oxidative stress, increase in intracellular calcium, and
cytosol to membrane PKC-II translocation (with no change
in PKC-
) were demonstrated after exposure to AGE-rich proteins.
These data support the hypothesis that AGEs cause mesangial oxidative
stress and alterations in PKC-II, changes that may
ultimately contribute to phenotypic abnormalities associated with
diabetic nephropathy.
advanced glycation end products; protein kinase C isoforms; intracellular oxidative stress; mesangial cells; neonatal rat mesangial cells
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