Normalization of hyperosmotic-induced inositol uptake by renal and endothelial cells is regulated by NF-κB

Mark A. Yorek*, Joyce A. Dunlap, Wenli Liu, William L. Lowe

*Corresponding author for this work

Research output: Contribution to journalArticle

11 Scopus citations

Abstract

Hyperosmolarity is a stress factor that has been shown to cause an increase in the transcription of the Na+-dependent myo-inositol cotransporter (SMIT). However, regulation of the reversion of SMIT mRNA levels and transporter activity following removal of hyperosmotic stress is less understood. Previously we have shown that postinduction normalization of SMIT mRNA levels and myo-inositol accumulation following removal of hyperosmotic stress is inhibited by actinomycin D and cycloheximide, suggesting that normalization requires RNA transcription and protein synthesis. We now demonstrate that removal of hyperosmotic stress causes an activation of the transcription factor NF-κB in renal and endothelial cells. Inhibiting NF-κB activation with pyrrolidine dithiocarbamate (PD) blocks the normalization of SMIT mRNA levels and myo-inositol accumulation on removal of the cells from hyperosmotic medium. These studies demonstrate that the downregulation of the myo-inositol transporter following reversal of hyperosmotic induction is regulated via the activation of NF-κB.

Original languageEnglish (US)
Pages (from-to)C1011-C1018
JournalAmerican Journal of Physiology - Cell Physiology
Volume278
Issue number5 47-5
DOIs
StatePublished - 2000

Keywords

  • Hyperosmolarity
  • Myo-inositol
  • Nuclear factor κB
  • Sodium-dependent myo- inositol cotransporter

ASJC Scopus subject areas

  • Physiology
  • Cell Biology

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