Specific Increase in p85α Expression in Response to Dexamethasone Is Associated with Inhibition of Insulin-like Growth Factor-I Stimulated Phosphatidylinositol 3-Kinase Activity in Cultured Muscle Cells

Giorgino, Francesco; Pedrini, Michael T.; Matera, Lucrezia; Smith, Robert J.

doi:10.1074/jbc.272.11.7455

Cited by 80Metabolism, Diabetes, and CancerPI3K/AKT/mTOR signaling in cancerMuscle Physiology and Disorders

Specific Increase in p85α Expression in Response to Dexamethasone Is Associated with Inhibition of Insulin-like Growth Factor-I Stimulated Phosphatidylinositol 3-Kinase Activity in Cultured Muscle Cells

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Giorgino, Francesco, Pedrini, Michael T., Matera, Lucrezia, Smith, Robert J.·1997·Journal of Biological Chemistry

DOI 10.1074/jbc.272.11.7455

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Abstract

The stimulation of phosphatidylinositol (PI) 3-kinase by insulin-like growth factor I (IGF-I) in L6 cultured skeletal muscle cells is inhibited by the glucocorticoid dexamethasone. The objective of this study was to investigate the mechanism of dexamethasone action by determining its effects on the expression of the p85alpha and p85beta regulatory subunit isoforms of PI 3-kinase, their coupling with the p110 catalytic subunit, and their association with insulin receptor substrate 1 (IRS-1) in response to IGF-I stimulation. Dexamethasone induced a 300% increase in p85alpha protein content in the L6 cultured myoblast cell line, whereas it increased p110 content by only 38% and had no effect on p85beta. The increase in p85alpha protein was associated with a coordinate increase in p85alpha mRNA. Stimulation with IGF-I induced the association of p85alpha and p85beta with IRS-1, and this was accompanied by increased amounts of the p110 catalytic subunit and markedly increased PI 3-kinase activity in IRS-1 immunoprecipitates. In cells treated with dexamethasone, greater amounts of p85alpha and lower amounts of p85beta, respectively, were found in IRS-1 immunoprecipitates, such that the alpha/beta ratio was markedly higher than in control cells. In spite of the increase in both total and IRS-1-associated p85alpha following dexamethasone treatment, IRS-1-associated p110 catalytic subunit and PI 3-kinase activity were decreased by approximately 50%. Thus, dexamethasone induces a specific increase in expression of the p85alpha regulatory subunit that is not associated with a coordinate increase in the p110 catalytic subunit of PI 3-kinase. As a consequence, in dexamethasone-treated cells, p85alpha that is not coupled with p110 competes with both p85alpha.p110 and p85beta.p110 complexes for association with IRS-1, leading to increased p85alpha but decreased p85beta, p110, and PI 3-kinase activity in IRS-1 immunoprecipitates.

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Binding of free p85α monomer to IRS-1 does not increase PI 3-kinase activity, but instead competes with binding of the p85α-p110 heterodimer, and consequently impairs PI 3-kinase activation.
“Binding of free p85α monomer to IRS-1 does not increase PI 3-kinase activity, but instead competes with binding of the p85α-p110 heterodimer, and consequently impairs PI 3-kinase activation [44].”
From Glucocorticoid-induced insulin resistance in skeletal muscles: defects in insulin signalling and the effects of a selective glycogen synthase kinase-3 inhibitor (2005) · cites this paper as [44]
p85α exists as a free monomer or bound to p110.
“It has been hypothesised that p85α exists as a free monomer or bound to p110 [44].”
From Glucocorticoid-induced insulin resistance in skeletal muscles: defects in insulin signalling and the effects of a selective glycogen synthase kinase-3 inhibitor (2005) · cites this paper as [44]

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Specific increase in p85alpha expression in response to dexamethasone is associated with inhibition of insulin-like growth factor-I stimulated phosphatidylinositol 3-kinase activity in cultured muscle cells.
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Authors: Giorgino, F., Pedrini, M. T., Matera, L., & Smith, R. J.
Affiliations: Brigham and Women's Hospital (US)
University of Bari Aldo Moro (IT)
Corresponding author: Smith, Robert J.
ORCID: Giorgino, Francesco
Smith, Robert J.
Venue: Journal of Biological Chemistry
Publisher: Elsevier BV
Published: 1997-03
Volume: 272
Issue: 11
Pages: 7455-7463
ISSN: 0021-9258 (ISSN-L)
DOI: 10.1074/jbc.272.11.7455
OpenAlex: W2064167816
Cited by: 80
References: 55
Citations by year: 2026: 1 · 2025: 1 · 2024: 1 · 2023: 2 · 2022: 3 · 2021: 2 · 2020: 2 · 2019: 2 · 2016: 2 · 2015: 2 · 2014: 1 · 2013: 4 · 2012: 4
FWCI: 0.95
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
creativecommons.org/licenses/by/4.0/ (vor, 8624 d)
Locations: Journal of Biological Chemistry (publishedVersion, cc-by)
PubMed (publishedVersion)
CINECA IRIS Institutional Research Information System (University of Bari Aldo Moro) (submittedVersion)
INFM-OAR (INFN Catania) (submittedVersion, other-oa)
Funders: Eli Lilly and Company
Max Kade Foundation
National Institutes of Health (5r01dk050411-10, 5r01dk048503-03, DK 36836)
National Institute of Diabetes and Digestive and Kidney Diseases (DK48503, R01DK043038, DK 50411, DK-43038)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
Keywords: dexamethasone, p85α, p85β, phosphatidylinositol 3-kinase, insulin-like growth factor I, IRS-1, p110 catalytic subunit, glucocorticoid regulation, skeletal muscle cells, L6 myoblasts, signal transduction inhibition
MeSH terms: Animals, Cell Line, Dexamethasone, Insulin-Like Growth Factor I, Gene Expression Regulation, Enzymologic, Phosphotransferases (Alcohol Group Acceptor), Muscle, Skeletal, Phosphatidylinositol 3-Kinases, Rats

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Specific Increase in p85α Expression in Response to Dexamethasone Is Associated with Inhibition of Insulin-like Growth Factor-I Stimulated Phosphatidylinositol 3-Kinase Activity in Cultured Muscle Cells

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