The DOI matches its Crossref record; 55 of the 56 references it cites were found in a registry or an index.
Species-specific glucocorticoid and 1,25-dihydroxyvitamin D responsiveness in mouse MC3T3–E1 osteoblasts: dexamethasone inhibits osteoblast differentiation and vitamin D down-regulates osteocalcin gene expression.
Abstract
The mouse MC3T3-E1 cell line is nontumorigenic and undergoes a typical program of osteoblast differentiation in vitro, producing a bone-like mineralized extracellular matrix. We report responses of these cells to dexamethasone (Dex) and 1,25-(OH)2D3 that are in contrast to findings from other osteoblast culture systems. First, chronic exposure of both early- and late-passaged MC3T3-E1 cells to 10(-7) M Dex, initiated during the proliferation period, blocked osteoblast differentiation, in contrast to the enhanced differentiation observed in cultures of fetal rat calvarial-derived cells. Secondly, 1,25-(OH)2D3 did not up-regulate expression (messenger RNA or protein synthesis) of the endogenous mouse osteocalcin (OC) gene. Several lines of evidence are presented that suggest this response is caused by sequence specific properties of the mouse OC vitamin D response element. We also observed both qualitative and quantitative differences in expression of cell growth (histone H2B) and phenotype-related genes (collagen, OC, osteopontin, glucocorticoid receptor, and 1, 25-(OH)2D3 receptor), between pre- and postmineralization stage osteoblasts, in response to 24 h steroid hormone treatment. Our findings in MC3T3-E1 cells are consistent with current concepts of selective influences of 1,25-(OH)2D3 and glucocorticoids as a function of osteoblast maturation. However, the inhibition of osteoblast differentiation by chronic Dex at 10(-7) M and the down-regulation of OC by 1,25-(OH)2D3 are novel observations relevant to species-specific responsiveness of mouse bone-expressed genes to steroid hormones during osteoblast differentiation.
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“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 [250]
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Metadata
- Authors
- Lian, J. B., Shalhoub, V., Aslam, F., Frenkel, B., Green, J., Hamrah, M., Stein, G. S., & Stein, J. L.
- Affiliations
- University of Massachusetts Chan Medical School (US)
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 1997-05-01
- Volume
- 138
- Issue
- 5
- Pages
- 2117-2127
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- OpenAlex
- W2169357450
- Cited by
- 154
- References
- 56
- Citations by year
- 2023: 3 · 2021: 3 · 2020: 2 · 2019: 1 · 2018: 3 · 2017: 3 · 2016: 4 · 2015: 3 · 2014: 2 · 2013: 6 · 2012: 10
- FWCI
- 3.90
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- The Journal of the American Medical Association (JAMA) Network (American Medical Association) (submittedVersion)
- Funders
- National Institutes of Health (5r01ar033920-12, 5r01dk046721-03)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK-46721)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR33920)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Vitamin D Research Studies
- Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
- Keywords
- glucocorticoids, 1,25-dihydroxyvitamin D3, dexamethasone, osteogenic differentiation, MC3T3-E1 cells, osteocalcin gene expression, vitamin D response element, osteoblast maturation, bone mineralization, glucocorticoid receptor, 1,25-dihydroxyvitamin D3 receptor, osteopontin, collagen, histone H2B
- MeSH terms
- Animals, Base Sequence, Calcitriol, Cell Differentiation, Cell Line, Dexamethasone, Glucocorticoids, Histones, Osteoblasts, Promoter Regions, Genetic, RNA, Messenger, Time Factors, Transfection, Osteocalcin, Gene Expression, Mice
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