Research Topics
Genomes and Genes
| CHARLES A O'BRIENSummaryAffiliation: University of Arkansas for Medical Sciences Country: USA Publications
Research Grants
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Detail Information
Publications
Osteocyte control of osteoclastogenesisCHARLES A O'BRIEN
Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences and the Central Arkansas Veterans Healthcare System, Little Rock, AR 72205, USA Electronic address
Bone 54:258-63. 2013..The goal of this review is to discuss these and other studies that reveal mechanisms whereby osteocytes control osteoclast formation and thus bone resorption. This article is part of a Special Issue entitled "The Osteocyte"...
IL-6 is not required for parathyroid hormone stimulation of RANKL expression, osteoclast formation, and bone loss in miceCHARLES A O'BRIEN
Division of Endocrinology and Metabolism, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
Am J Physiol Endocrinol Metab 289:E784-93. 2005..These results demonstrate that IL-6 is not required for the osteoclast formation and bone loss that accompanies continuous elevation of PTH...- Parathyroid hormone controls receptor activator of NF-kappaB ligand gene expression via a distant transcriptional enhancerQiang Fu
University of Arkansas for Medical Sciences, 4301 W Markham St, Mail Slot 587, Little Rock, AR 72205, USA
Mol Cell Biol 26:6453-68. 2006..Thus, PTH responsiveness of the RANKL gene is determined by a distant regulatory region that responds to cAMP in a cell-type-specific manner and Runx2 may contribute to such cell-type specificity... - Control of RANKL gene expressionCHARLES A O'BRIEN
Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, and Central Arkansas Veterans Healthcare System, Little Rock, AR 72205, USA
Bone 46:911-9. 2010.... - Control of bone mass and remodeling by PTH receptor signaling in osteocytesCHARLES A O'BRIEN
Division of Endocrinology, Center for Osteoporosis and Metabolic Bone Diseases, Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States of America
PLoS ONE 3:e2942. 2008..These findings demonstrate that PTH receptor signaling in osteocytes increases bone mass and the rate of bone remodeling through LRP5-dependent and -independent mechanisms, respectively... - Estrogen receptor-α signaling in osteoblast progenitors stimulates cortical bone accrualMaria Almeida
Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences and Central Arkansas Veterans Healthcare System, Little Rock, Arkansas, USA
J Clin Invest 123:394-404. 2013..Hence, the ERα in both osteoblast progenitors and osteoclasts functions to optimize bone mass but at distinct bone compartments and in response to different cues... - Estrogens attenuate oxidative stress and the differentiation and apoptosis of osteoblasts by DNA-binding-independent actions of the ERalphaMaria Almeida
Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences and Central Arkansas Veterans Health Care System, Little Rock, AR, USA
J Bone Miner Res 25:769-81. 2010.... - Skeletal involution by age-associated oxidative stress and its acceleration by loss of sex steroidsMaria Almeida
Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, 4301 West Markham, Little Rock, AR 72205, USA
J Biol Chem 282:27285-97. 2007..Loss of estrogens or androgens accelerates the effects of aging on bone by decreasing defense against oxidative stress... - The estrogen receptor-alpha in osteoclasts mediates the protective effects of estrogens on cancellous but not cortical boneMarta Martin-Millan
Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences and the Central Arkansas Veterans Healthcare System, Little Rock, Arkansas 72205 7199, USA
Mol Endocrinol 24:323-34. 2010..However, additional effects of estrogens on osteoblasts, osteocytes, and perhaps other cell types are required for their protective effects on the cortical compartment, which constitutes 80% of the skeleton... - Proteasomal degradation of Runx2 shortens parathyroid hormone-induced anti-apoptotic signaling in osteoblasts. A putative explanation for why intermittent administration is needed for bone anabolismTeresita Bellido
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, Arkansas 72205, USA
J Biol Chem 278:50259-72. 2003..The self-limiting nature of PTH-induced survival signaling might explain why intermittent administration of the hormone is required for bone anabolism... - PTH receptor signaling in osteocytes governs periosteal bone formation and intracortical remodelingYumie Rhee
Department of Anatomy and Cell Biology, Division of Endocrinology, Indiana University School of Medicine, Indianapolis, IN 46202, USA
J Bone Miner Res 26:1035-46. 2011..These findings demonstrate that PTH receptor signaling influences cortical bone through actions on osteocytes and defines the role of Wnt signaling in PTH receptor action... - Targeted deletion of a distant transcriptional enhancer of the receptor activator of nuclear factor-kappaB ligand gene reduces bone remodeling and increases bone massCarlo Galli
Center for Osteoporosis and Metabolic Bone Disease, University of Arkansas for Medical Sciences, 4301 West Markham Street, MS 587, Little Rock, Arkansas 72205, USA
Endocrinology 149:146-53. 2008..These findings demonstrate that hormonal control of RANKL expression via the DCR is a critical determinant of the rate of bone remodeling... - The RANKL distal control region is required for the increase in RANKL expression, but not the bone loss, associated with hyperparathyroidism or lactation in adult miceMelda Onal
Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
Mol Endocrinol 26:341-8. 2012.... - Receptor activator of nuclear factor κB ligand (RANKL) protein expression by B lymphocytes contributes to ovariectomy-induced bone lossMelda Onal
Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
J Biol Chem 287:29851-60. 2012..These results demonstrate that lymphocyte RANKL is not involved in basal bone remodeling, but B cell RANKL does contribute to the increase in osteoclasts and cancellous bone loss that occurs after loss of estrogen... - Matrix-embedded cells control osteoclast formationJinhu Xiong
Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences UAMS, Little Rock, Arkansas, USA
Nat Med 17:1235-41. 2011..These results suggest that the rate-limiting step of matrix resorption is controlled by cells embedded within the matrix itself... - Continuous elevation of PTH increases the number of osteoblasts via both osteoclast-dependent and -independent mechanismsRobert L Jilka
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, AR 72205, USA
J Bone Miner Res 25:2427-37. 2010..These results indicate that PTH stimulates osteoclast-dependent as well as osteoclast-independent (Wnt signaling) pro-osteoblastogenic pathways, both of which are required for balanced focal bone remodeling in cancellous bone... - Osteoprotegerin prevents glucocorticoid-induced osteocyte apoptosis in miceRobert S Weinstein
Division of Endocrinology and Metabolism, Central Arkansas Veterans Healthcare System and University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
Endocrinology 152:3323-31. 2011..Based on these results, we conclude that at least part of the OPG-induced preservation of bone strength is due to the maintenance of osteocyte viability and the lacunar-canalicular network... - FoxO-mediated defense against oxidative stress in osteoblasts is indispensable for skeletal homeostasis in miceElena Ambrogini
Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences and the Central Arkansas Veterans Healthcare System, Little Rock, AR 72205, USA
Cell Metab 11:136-46. 2010..We conclude that FoxO-dependent oxidative defense provides a mechanism to handle the oxygen free radicals constantly generated by the aerobic metabolism of osteoblasts and is thereby indispensable for bone mass homeostasis... - Endogenous glucocorticoids decrease skeletal angiogenesis, vascularity, hydration, and strength in aged miceRobert S Weinstein
Center for Osteoporosis and Metabolic Bone Diseases, Department of Internal Medicine, Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock, USA
Aging Cell 9:147-61. 2010.... - A novel ligand-independent function of the estrogen receptor is essential for osteocyte and osteoblast mechanotransductionJ Ignacio Aguirre
Division of Endocrinology and Metabolism, the Center for Osteoporosis and Metabolic Bone Diseases, The Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
J Biol Chem 282:25501-8. 2007.... - Commitment to the osteoblast lineage is not required for RANKL gene expressionCarlo Galli
Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, and Central Arkansas Veterans Healthcare System, Little Rock, AR 72205, USA
J Biol Chem 284:12654-62. 2009.... - Intermittent PTH stimulates periosteal bone formation by actions on post-mitotic preosteoblastsRobert L Jilka
Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, Central Arkansas Veterans Healthcare System, Slot 587, University of Arkansas for Medical Sciences, 4301 W Markham, Little Rock, AR, USA
Bone 44:275-86. 2009..Targeting the latter cells is an effective mechanism for increasing osteoblast number in periosteal bone where the production of osteoblasts from replicating progenitors is slow... - Glucocorticoids act directly on osteoblasts and osteocytes to induce their apoptosis and reduce bone formation and strengthCHARLES A O'BRIEN
Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, Department of Internal Medicine, Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock 72205 7199, USA
Endocrinology 145:1835-41. 2004..Furthermore, our results suggest that glucocorticoid-induced loss of bone strength results in part from increased death of osteocytes, independent of bone loss... - Parathyroid hormone stimulates receptor activator of NFkappa B ligand and inhibits osteoprotegerin expression via protein kinase A activation of cAMP-response element-binding proteinQiang Fu
Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Little Rock 72205, USA
J Biol Chem 277:48868-75. 2002..These results demonstrate that PTH directly stimulates RANKL expression via a PKA-CREB pathway and that CREB may be a central regulator of RANKL expression. Furthermore, they suggest that PTH suppression of OPG involves CREB and c-fos... - Oxidative stress antagonizes Wnt signaling in osteoblast precursors by diverting beta-catenin from T cell factor- to forkhead box O-mediated transcriptionMaria Almeida
Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences and the Central Arkansas Veterans Healthcare System, Little Rock, AR 72205, USA
J Biol Chem 282:27298-305. 2007.... - Osteocyte RANKL: new insights into the control of bone remodelingJinhu Xiong
Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
J Bone Miner Res 27:499-505. 2012..The goal of this review is to highlight the results of these new studies and discuss their implications for our understanding of bone remodeling...
Research Grants
- MOLECULAR CONTROL OF RANKL GENE EXPRESSIONCHARLES O BRIEN; Fiscal Year: 2009....
- MOLECULAR CONTROL OF RANKL GENE EXPRESSIONCHARLES O BRIEN; Fiscal Year: 2007..Information gained from these studies will lead to a better understanding of the cellular factors involved in the support of osteoclast formation and thereby identify novel targets for anti-resorptive therapy. ..
- IN VIVO REGULATION OF IL6 AND IL6R GENE EXPRESSIONCHARLES O BRIEN; Fiscal Year: 2002..Finally, cis-acting regulatory elements in the IL-6 promoter that are the targets for estrogen and PTH actions in vivo will be identified. ..
- MOLECULAR CONTROL OF RANKL GENE EXPRESSIONCHARLES A O apos BRIEN; Fiscal Year: 2010....