ERK and p38 mediate high-glucose-induced hypertrophy and TGF-β expression in renal tubular cells

Hisayo Fujita, Sayu Omori, Kenji Ishikura, Mariko Hida, Midori Awazu

Research output: Contribution to journalArticlepeer-review

109 Citations (Scopus)

Abstract

We investigated the expression of ERK, p38 mitogen-activated protein kinase (p38), and JNK in renal tubules of diabetic rats following 3 wk after streptozotocin injection (DM). Although the expression of ERK was not different between controls and DM, phosphorylated ERK was expressed more intensely in DM. p38 And phosphorylated p38 were detected only in the diabetic kidney and were localized in all tubular segments. JNK and phosphorylated JNK were expressed similarly in controls and DM. Transforming growth factor (TGF)-β was expressed in all tubular segments of DM, coinciding with the localization of p38. In LLC-PK1 cells, phosphorylation of ERK and p38 increased after 24- to 72-h exposure to high glucose (HG). Coincubation with a p38 inhibitor SB-203580 or a MEK inhibitor, PD-98059, suppressed the HG-induced increases in protein content, [3H]leucine incorporation, and the protein-to-DNA ratio. SB-203580 or PD-98059 also abolished the HG-stimulated expression of TGF-β protein. These results demonstrate that ERK and p38 are activated in renal tubular cells of DM and may mediate HG-induced cellular hypertrophy and TGF-β expression.

Original languageEnglish
Pages (from-to)F120-F126
JournalAmerican Journal of Physiology - Renal Physiology
Volume286
Issue number1 55-1
Publication statusPublished - 2004 Jan 1

Keywords

  • Diabetes
  • Kidney
  • Mitogen-activated protein kinase

ASJC Scopus subject areas

  • Physiology
  • Urology

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