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The repair of Na + ‐dependent glucose uptake following injury is regulated by PKC‐α and PKC‐ε .
Author(s) -
Nowak Grazyna,
Bakajsova Diana
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a506-d
Subject(s) - protein kinase c , chemistry , glucose uptake , reabsorption , microbiology and biotechnology , medicine , endocrinology , kinase , kidney , biology , biochemistry , insulin
Na + ‐dependent glucose transport is the major mechanism responsible for glucose reabsorption by the proximal tubule segment of the nephron. The repair of Na + ‐coupled glucose transport following injury is critical for restoration of normal renal function. This study tested a hypothesis that protein kinase C (PKC) regulates the repair of Na + ‐coupled glucose uptake in renal proximal tubular cells (RPTC) following oxidant‐induced injury. RPTC were grown in primary culture and injured by treating with the oxidant tert‐butylhydroperoxide (0.35 mM, 40 min). Na + ‐coupled glucose uptake decreased to 19% of controls following injury, improved on day 4 (61% of control) and recovered on day 6. Oxidant injury activated PKC‐α and PKC‐ε in RPTC. Overexpressing dominant negative (inactive) PKC‐α decreased Na + ‐coupled glucose uptake in non‐injured RPTC (56% of control) and reduced the recovery of this function (44% of control). Overexpressing wild type PKC‐α had no effect. Overexpressing dominant negative PKC‐ε reduced the decreases in Na + ‐coupled glucose uptake (43% of control) and resulted in repair of this function 4 days after the injury. In contrast, overexpressing constitutively active PKC‐ε blocked the recovery of Na + ‐coupled glucose uptake (16% of control). We conclude that activation of PKC‐α promotes, whereas activation of PKC‐ε blocks the repair of Na + ‐coupled glucose uptake in oxidant‐injured RPTC.