Glucocorticoids inhibit the attachment of osteoblasts to bone extracellular matrix proteins and decrease beta 1-integrin levels.

Gronowicz, G A; McCarthy, M B

doi:10.1210/endo.136.2.7530648

Cited by 87Bone Metabolism and DiseasesCell Adhesion Molecules ResearchBone and Dental Protein Studies

Glucocorticoids inhibit the attachment of osteoblasts to bone extracellular matrix proteins and decrease beta 1-integrin levels.

Gronowicz, G A, McCarthy, M B·1995·Endocrinology

DOI 10.1210/endo.136.2.7530648

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Abstract

Prolonged glucocorticoid treatment causes osteoporosis in vivo and inhibits bone formation in vitro. We have previously shown that glucocorticoids inhibit calcification and alter osteoblast organization in a mineralizing bone organ culture system. In this study, the effect of glucocorticoids on osteoblast adhesion to bone matrix proteins and integrin expression was examined in primary rat osteoblasts and a transformed rat osteosarcoma-derived cell line ROS 17/2.8. After 24 h of treatment with corticosterone, these cells displayed a concentration-dependent decrease in adhesion to type I collagen and fibronectin. Adhesion was significantly decreased as early as 4 h after glucocorticoid administration. With 100 nM corticosterone treatment for 24 h, inhibition of the adhesion of ROS 17/2.8 cells and primary osteoblasts to fibronectin was 75 +/- 10% and 50 +/- 8%, and inhibition of adhesion to collagen was 31 +/- 10% and 65 +/- 5%, respectively. This effect was specific for osteoblasts, because glucocorticoids did not change the adhesion of fibroblasts. However, glucocorticoids did inhibit the adhesion of all cell types to rat osteonectin. To determine whether the change in osteoblast attachment to collagen and fibronectin was due to an alteration in integrin levels, the plasma membranes of these cells were labeled with [125I]lactoperoxidase, solubilized, and immunoprecipitated with an antibody to beta 1. A 24-h treatment with 100 nM corticosterone caused 80 +/- 2% and 64 +/- 9% decreases in beta 1 levels in primary osteoblasts and ROS 17/2.8 cells, respectively. These results were confirmed with immunofluorescence microscopy, which showed a glucocorticoid-induced decrease in beta 1 staining. Treatment of primary rat osteoblasts and ROS 17/2.8 cells for 72 h with corticosterone also decreased beta 1-integrin messenger RNA levels in a dose-dependent manner. We have demonstrated that the inhibition of integrin expression by glucocorticoids is involved in the decrease in osteoblast adhesion to bone extracellular matrix proteins. These data suggest that integrin modulation may influence osteoblast function and bone formation and, thus, contribute to glucocorticoid-induced osteoporosis.

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Glucocorticoids can inhibit osteoblast differentiation, attachment to bone matrix, and production of IGF-I.
“Glucocorticoids can also inhibit osteoblast differentiation (249 -251), osteoblast attachment to bone matrix (252), and osteoblast production of IGF-I (253).”
From Receptor Activator of Nuclear Factor κB Ligand and Osteoprotegerin Regulation of Bone Remodeling in Health and Disease (2008) · cites this paper as [252]

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Authors: Gronowicz, G. A., & McCarthy, M. B.
Affiliations: UConn Health (US)
ORCID: Gronowicz, G A
Venue: Endocrinology
Publisher: The Endocrine Society
Published: 1995-02
Volume: 136
Issue: 2
Pages: 598-608
ISSN: 0013-7227 (ISSN-L)
1945-7170
DOI: 10.1210/endo.136.2.7530648
OpenAlex: W2117224996
Cited by: 87
References: 35
Citations by year: 2026: 1 · 2019: 1 · 2017: 1 · 2016: 2 · 2015: 1 · 2014: 3 · 2013: 1 · 2012: 1
FWCI: 2.60
Type: journal article
Language: en
Open access: closed
Locations: Endocrinology (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (5r29ar038636-05)
National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR38636)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
Health Sciences › Medicine › Rheumatology › Bone and Dental Protein Studies
Keywords: glucocorticoids, corticosterone, osteoblast adhesion, beta1 integrin, type I collagen, fibronectin, SPARC, bone matrix, osteoporosis, bone formation, ROS 17/2.8 cells, fibroblast adhesion
MeSH terms: Animals, Bone and Bones, Cell Adhesion, Cell Line, Cell Membrane, Collagen, Corticosterone, Fibronectins, Fluorescent Antibody Technique, Osteoblasts, Precipitin Tests, RNA, Messenger, Osteosarcoma, Osteonectin, Integrins, Extracellular Matrix Proteins, Bone Remodeling, Integrin beta1, Rats

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Glucocorticoids inhibit the attachment of osteoblasts to bone extracellular matrix proteins and decrease beta 1-integrin levels.

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