Research Topics
| S C ManolagasSummaryAffiliation: University of Arkansas for Medical Sciences Country: USA Publications
| Collaborators
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Detail Information
Publications
Birth and death of bone cells: basic regulatory mechanisms and implications for the pathogenesis and treatment of osteoporosisS C Manolagas
Division of Endocrinology and Metabolism, University of Arkansas for Medical Sciences, Little Rock 72205, USA
Endocr Rev 21:115-37. 2000....- Reversal of bone loss in mice by nongenotropic signaling of sex steroidsS Kousteni
Division of Endocrinology and Metabolism, Department of Internal Medicine, and Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
Science 298:843-6. 2002..Such ligands merit investigation as potential therapeutic alternatives to hormone replacement for osteoporosis in both women and men [corrected]... 
Attenuation of the self-renewal of transit-amplifying osteoblast progenitors in the murine bone marrow by 17 beta-estradiolG B Di Gregorio
Division of Endocrinology and Metabolism, Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
J Clin Invest 107:803-12. 2001....- Inhibition of osteoblastogenesis and promotion of apoptosis of osteoblasts and osteocytes by glucocorticoids. Potential mechanisms of their deleterious effects on boneR S Weinstein
Division of Endocrinology Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, and the McClellan Veterans Affairs Medical Center GRECC, Little Rock, Arkansas 72205, USA
J Clin Invest 102:274-82. 1998..Furthermore, accumulation of apoptotic osteocytes may contribute to osteonecrosis. These findings provide evidence that glucocorticoid-induced bone disease arises from changes in the numbers of bone cells... - Nongenotropic, sex-nonspecific signaling through the estrogen or androgen receptors: dissociation from transcriptional activityS Kousteni
Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic, Bone Diseases, University of Arkansas for Medical Sciences and, the Central Arkansas Veterans Health Care, System, Little Rock, AR 72205, USA
Cell 104:719-30. 2001.... - Chronic elevation of parathyroid hormone in mice reduces expression of sclerostin by osteocytes: a novel mechanism for hormonal control of osteoblastogenesisT Bellido
Division of Endocrinology and Metabolism, and Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, 4301 West Markham, Little Rock, Arkansas 72205, USA
Endocrinology 146:4577-83. 2005.... - Breast cancer increases osteoclastogenesis by secreting M-CSF and upregulating RANKL in stromal cellsA T Mancino
Department of Surgery, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
J Surg Res 100:18-24. 2001..The ability to stimulate osteoclasts may explain the ability to metastasize to bone... - The effects of androgen deficiency on murine bone remodeling and bone mineral density are mediated via cells of the osteoblastic lineageR S Weinstein
Division of Endocrinology Metabolism, McClellan Veterans Affairs Medical Center Geriatric Research, Education, and Clinical Center, University of Arkansas for Medical Sciences, Little Rock 72205, USA
Endocrinology 138:4013-21. 1997..This evidence suggests that cells of the osteoblastic lineage are essential mediators of the changes in the rate of bone remodeling and loss of bone mass that ensue following loss of androgens... - Activation of the Janus kinase/STAT (signal transducer and activator of transcription) signal transduction pathway by interleukin-6-type cytokines promotes osteoblast differentiationT Bellido
Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, and the McClellan Veterans Administration Medical Center, Little Rock 72205, USA
Endocrinology 138:3666-76. 1997.... - Expression levels of gp130 in bone marrow stromal cells determine the magnitude of osteoclastogenic signals generated by IL-6-type cytokinesC A O'Brien
Division of Endocrinology and Metabolism, Department of Medicine, Center for Osteoporosis and Metabolic Bone Diseases, and the McClellan VAMC, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
J Cell Biochem 79:532-41. 2000.... - Increased bone formation by prevention of osteoblast apoptosis with parathyroid hormoneR L Jilka
Division of Endocrinology and Metabolism, UAMS Center for Osteoporosis and Metabolic Bone Diseases, and Central Arkansas Veterans Health Care System, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
J Clin Invest 104:439-46. 1999..Moreover, it suggests novel pharmacotherapeutic strategies for osteoporosis and, perhaps, other pathologic conditions in which tissue mass diminution has compromised functional integrity... - Classical genotropic versus kinase-initiated regulation of gene transcription by the estrogen receptor alphaM Almeida
Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock, 72205, USA
Endocrinology 147:1986-96. 2006..These results support an extensive divergence in gene expression depending on the mode of ER activation... - Meltrin-alpha, a fusion protein involved in multinucleated giant cell and osteoclast formationE Abe
Division of Endocrinology and Metabolism, John L McClellan VA Geriatric Research, Education, and Clinical Center, University of Arkansas for Medical Sciences, Little Rock 72205, USA
Calcif Tissue Int 64:508-15. 1999..These observations demonstrate that meltrins play a role in MGC and osteoclast formation from mononuclear precursors, as in the case with myotubes... - Glucocorticoids act directly on osteoclasts to increase their life span and reduce bone densityD Jia
Department of Internal Medicine, and the Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, 4301 West Markham Street, Slot 587, Little Rock, Arkansas 72205, USA
Endocrinology 147:5592-9. 2006..These results demonstrate for the first time that the early, rapid loss of bone caused by glucocorticoid excess results from direct actions on osteoclasts... - Inhibition of Osf2/Cbfa1 expression and terminal osteoblast differentiation by PPARgamma2B Lecka-Czernik
Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, Little Rock, Arkansas 72205, USA
J Cell Biochem 74:357-71. 1999..These results strongly suggest that PPARgamma2 negatively regulates stromal cell plasticity by suppressing Osf2/Cbfa1 and osteoblast-like biosynthetic activity, while promoting terminal differentiation to adipocytes... - Inhibin suppresses and activin stimulates osteoblastogenesis and osteoclastogenesis in murine bone marrow culturesD Gaddy-Kurten
Department of Physiology and Biophysics, Division of Endocrinology, University of Arkansas for Medical Sciences, 4301 West Markham, Little Rock, AR 72205, USA
Endocrinology 143:74-83. 2002.... - Cbfa1 does not regulate RANKL gene activity in stromal/osteoblastic cellsC A O'Brien
Division of Endocrinology and Metabolism, Department of Medicine, Center for Osteoporosis and Metabolic Bone Diseases, and the Central Arkansas Healthcare System, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
Bone 30:453-62. 2002.... - Sex steroids and boneS C Manolagas
Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Little Rock 72205, USA
Recent Prog Horm Res 57:385-409. 2002..The same ligands may also circumvent the side effects associated with conventional hormone replacement therapy... - STAT3 activation in stromal/osteoblastic cells is required for induction of the receptor activator of NF-kappaB ligand and stimulation of osteoclastogenesis by gp130-utilizing cytokines or interleukin-1 but not 1,25-dihydroxyvitamin D3 or parathyroid hormC A O'Brien
Departments of Medicine and Pediatrics, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
J Biol Chem 274:19301-8. 1999..In addition, this study demonstrates that activation of the gp130-STAT3 pathway in stromal/osteoblastic cells mediates the osteoclastogenic effects of IL-1, but not parathyroid hormone or 1, 25-dihydroxyvitamin D3... - Transcriptional activation of the p21(WAF1,CIP1,SDI1) gene by interleukin-6 type cytokines. A prerequisite for their pro-differentiating and anti-apoptotic effects on human osteoblastic cellsT Bellido
Division of Endocrinology and Metabolism, the Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
J Biol Chem 273:21137-44. 1998..These results demonstrate that p21 is a downstream effector of gp130/Stat3 activation and a critical mediator of the pro-differentiating and anti-apoptotic effects of IL-6 type cytokines on human osteoblastic cells... - Apoptosis of osteocytes in glucocorticoid-induced osteonecrosis of the hipR S Weinstein
Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock 72205 7199, USA
J Clin Endocrinol Metab 85:2907-12. 2000.... - Calbindin-D28k is expressed in osteoblastic cells and suppresses their apoptosis by inhibiting caspase-3 activityT Bellido
Division of Endocrinology and Metabolism, the Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, and Central Arkansas Veteterans Health Care System, Little Rock, Arkansas 72205, USA
J Biol Chem 275:26328-32. 2000.... - Mechanical stimulation prevents osteocyte apoptosis: requirement of integrins, Src kinases, and ERKsL I Plotkin
Div. of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
Am J Physiol Cell Physiol 289:C633-43. 2005.... - Osteopontin expression by osteoclast and osteoblast progenitors in the murine bone marrow: demonstration of its requirement for osteoclastogenesis and its increase after ovariectomyT Yamate
Department of Medicine, UAMS Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Little Rock 72205, USA
Endocrinology 138:3047-55. 1997..These findings indicate that osteopontin is expressed during the early stages of the differentiation of osteoclast and osteoblast progenitors in the bone marrow and that its cell adhesion properties are required for osteoclastogenesis... - Chromosomal mapping of osteopenia-associated quantitative trait loci using closely related mouse strainsH Benes
Department of Biochemistry and Molecular Biology, University of Arkansas for Medical Sciences, Little Rock, USA
J Bone Miner Res 15:626-33. 2000..Such recurrent appearance of QTLs, especially in crosses involving distantly-related strains, implies that polymorphism at these loci may be favored by evolution and might underlie variation in peak bone density among humans... - Regulation of interleukin-6, osteoclastogenesis, and bone mass by androgens. The role of the androgen receptorT Bellido
Division of Endocrinology and Metabolism, University of Arkansas for Medical Sciences, Little Rock 72205, USA
J Clin Invest 95:2886-95. 1995.... - Essential requirement of BMPs-2/4 for both osteoblast and osteoclast formation in murine bone marrow cultures from adult mice: antagonism by nogginE Abe
Division of Endocrinology and Metabolism and the UAMS Center for Osteoporosis and Metabolic Bone Diseases, Little Rock, Arkansas, USA
J Bone Miner Res 15:663-73. 2000..Hence, BMPs, perhaps in balance with noggin and possibly other antagonists, may provide the tonic baseline control of the rate of bone remodeling on which other inputs (e.g., hormonal, biomechanical, etc.) operate...