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Am J Physiol Renal Physiol 281: F613-F619, 2001;
0363-6127/01 $5.00
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Vol. 281, Issue 4, F613-F619, October 2001

Activation of PKC-beta I in glomerular mesangial cells is associated with specific NF-kappa B subunit translocation

Anoop Kumar, Karen S. Hawkins, Meredith A. Hannan, and Michael B. Ganz

Division of Nephrology, Veterans Affairs Medical Center, and Section of Nephrology, Department of Medicine, Case Western Reserve University, Cleveland, Ohio 44106

Changes in expression and activity of protein kinase C (PKC) isoforms and early transcription factors may account for alterations in cell behavior seen in diabetes. We studied the expression of PKC-beta I in rat glomerular mesangial cells (MCs) cultured in normal or high glucose and compared it with the temporal and spatial expression of dimeric transcription factor (NF-kappa B) p50 and p65. The results show that in unstimulated cells PKC-beta I and NF-kappa B p50 are distributed in the cytosol and, on stimulation, their distribution is perinuclear and they are localized to the membrane. Serum-starved MCs cultured in high-glucose medium exhibit a predominantly cytosolic localization of PKC-beta I and both p50 and p65 NF-kappa B. However, phorbol 12-myristate 13-acetate (PMA) stimulation of cells grown in the presence of high glucose resulted in membrane translocation of PKC-beta I that was associated with nuclear translocation of NF-kappa B p65, but not NF-kappa B p50. Moreover, the translocation to the nucleus for NF-kappa B p65 was significantly higher in MCs exposed to high glucose compared with those exposed to normal glucose. These observations indicate that the NF-kappa B p65, but not NF-kappa B p50, expression and translocation pattern mirrors that of PKC-beta I, which may be one important pathway by which signaling is enhanced in the high-glucose state.

protein kinase C; transcriptional factors; diabetes; nephropathy


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