Wortmannin and LY294002 inhibit myo-inositol accumulation by cultured bovine aorta endothelial cells and murine 3T3-L1 adipocytes

Mark A Yorek; Joyce A Dunlap; William L Lowe

doi:10.1016/S0167-4889(00)00070-7

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Wortmannin and LY294002 inhibit myo-inositol accumulation by cultured bovine aorta endothelial cells and murine 3T3-L1 adipocytes

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Wortmannin and LY294002 inhibit myo-inositol accumulation by cultured bovine aorta endothelial cells and murine 3T3-L1 adipocytes

Mark A Yorek, Joyce A Dunlap and William L Lowe

Biochimica et biophysica acta. Molecular cell research, Vol.1497(3), pp.328-340

2000

DOI: 10.1016/S0167-4889(00)00070-7

PMID: 10996657

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Abstract

We have previously reported that myo-inositol uptake and metabolism is reduced in human fibroblasts derived from patients with ataxia telangiectasia (AT). Treating normal fibroblasts with 10–100 μM wortmannin duplicates some of the phenotypic properties of AT fibroblasts including the decrease in myo-inositol accumulation. In the present study we examined whether treatment of other types of mammalian cells with wortmannin or LY294002 altered myo-inositol uptake. Cultured bovine aorta endothelial cells or 3T3-L1 adipocytes were incubated with either wortmannin or LY294002, and afterwards, myo-inositol uptake and SMIT mRNA levels were determined. Incubating cultured bovine aorta endothelial cells and 3T3-L1 adipocytes with either wortmannin or LY294002 caused a time- and concentration-dependent decrease in myo-inositol accumulation that was independent of changes in SMIT mRNA levels. The effect of wortmannin and LY294002 on myo-inositol accumulation was not due to an increase in myo-inositol secretion. The effect of LY294002 on myo-inositol accumulation was reversible. Furthermore, the LY294002-induced decrease in myo-inositol accumulation was specific since the uptake of serine or choline by cultured bovine aorta endothelial cells and 3T3-L1 adipocytes treated with LY294002 was not significantly decreased. Co-incubation of cultured bovine aorta endothelial cells and 3T3-L1 adipocytes with either wortmannin or LY294002 and hyperosmotic medium caused a significant decrease in the induction of myo-inositol accumulation by hyperosmolarity without significantly affecting the hyperosmotic-induced increase in SMIT mRNA levels. These data suggest that myo-inositol accumulation is regulated post-translationally by wortmannin and LY294002.

LY29002

Phosphatidylinositol 3-kinase

Adipocytes

Wortmannin

Endothelial cells

myo-inositol

Details

Title: Subtitle: Wortmannin and LY294002 inhibit myo-inositol accumulation by cultured bovine aorta endothelial cells and murine 3T3-L1 adipocytes
Creators: Mark A Yorek - Department of Internal Medicine, Diabetes–Endocrinology Research Center and Veterans Affairs Medical Center (3 E 17), University of Iowa, Iowa City, IA 52246, USA
Joyce A Dunlap - Department of Internal Medicine, Diabetes–Endocrinology Research Center and Veterans Affairs Medical Center (3 E 17), University of Iowa, Iowa City, IA 52246, USA
William L Lowe - Department of Medicine, Veterans Affairs Lakeside Medical Center, and Northwestern University Medical School, Chicago, IL 60611, USA
Resource Type: Journal article
Publication Details: Biochimica et biophysica acta. Molecular cell research, Vol.1497(3), pp.328-340
DOI: 10.1016/S0167-4889(00)00070-7
PMID: 10996657
NLM abbreviation: Biochim Biophys Acta Mol Cell Res
ISSN: 0167-4889
eISSN: 1879-2596
Publisher: Elsevier B.V
Language: English
Date published: 2000
Academic Unit: Fraternal Order of Eagles Diabetes Research Center; Endocrinology and Metabolism; Internal Medicine
Record Identifier: 9984094607902771

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