CHARLES A O'BRIEN

Summary

Affiliation: University of Arkansas for Medical Sciences
Country: USA

Publications

  1. pmc Matrix-embedded cells control osteoclast formation
    Jinhu 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
  2. pmc Osteocyte control of osteoclastogenesis
    CHARLES 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
    Bone 54:258-63. 2013
  3. pmc Control of bone mass and remodeling by PTH receptor signaling in osteocytes
    CHARLES 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
  4. ncbi request reprint IL-6 is not required for parathyroid hormone stimulation of RANKL expression, osteoclast formation, and bone loss in mice
    CHARLES 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
  5. pmc Parathyroid hormone controls receptor activator of NF-kappaB ligand gene expression via a distant transcriptional enhancer
    Qiang 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
  6. pmc Control of RANKL gene expression
    CHARLES 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
  7. pmc FOXOs attenuate bone formation by suppressing Wnt signaling
    Srividhya Iyer
    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, USA
    J Clin Invest 123:3409-19. 2013
  8. pmc The estrogen receptor-alpha in osteoclasts mediates the protective effects of estrogens on cancellous but not cortical bone
    Marta 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
  9. pmc Estrogen receptor-α signaling in osteoblast progenitors stimulates cortical bone accrual
    Maria 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
  10. pmc Estrogens attenuate oxidative stress and the differentiation and apoptosis of osteoblasts by DNA-binding-independent actions of the ERalpha
    Maria 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

Research Grants

  1. IN VIVO REGULATION OF IL6 AND IL6R GENE EXPRESSION
    CHARLES O BRIEN; Fiscal Year: 1999
  2. MOLECULAR CONTROL OF RANKL GENE EXPRESSION
    CHARLES O BRIEN; Fiscal Year: 2007
  3. MOLECULAR CONTROL OF RANKL GENE EXPRESSION
    CHARLES O BRIEN; Fiscal Year: 2005
  4. MOLECULAR CONTROL OF RANKL GENE EXPRESSION
    CHARLES O BRIEN; Fiscal Year: 2004
  5. MOLECULAR CONTROL OF RANKL GENE EXPRESSION
    CHARLES O BRIEN; Fiscal Year: 2003
  6. IN VIVO REGULATION OF IL6 AND IL6R GENE EXPRESSION
    CHARLES O BRIEN; Fiscal Year: 2002
  7. IN VIVO REGULATION OF IL6 AND IL6R GENE EXPRESSION
    CHARLES O BRIEN; Fiscal Year: 2001
  8. MOLECULAR CONTROL OF RANKL GENE EXPRESSION
    CHARLES A O apos BRIEN; Fiscal Year: 2010
  9. MOLECULAR CONTROL OF RANKL GENE EXPRESSION
    CHARLES O BRIEN; Fiscal Year: 2006
  10. IN VIVO REGULATION OF IL6 AND IL6R GENE EXPRESSION
    CHARLES O BRIEN; Fiscal Year: 2000

Collaborators

Detail Information

Publications33

  1. pmc Matrix-embedded cells control osteoclast formation
    Jinhu 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...
  2. pmc Osteocyte control of osteoclastogenesis
    CHARLES 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
    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...
  3. pmc Control of bone mass and remodeling by PTH receptor signaling in osteocytes
    CHARLES 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...
  4. ncbi request reprint IL-6 is not required for parathyroid hormone stimulation of RANKL expression, osteoclast formation, and bone loss in mice
    CHARLES 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...
  5. pmc Parathyroid hormone controls receptor activator of NF-kappaB ligand gene expression via a distant transcriptional enhancer
    Qiang 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...
  6. pmc Control of RANKL gene expression
    CHARLES 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
    ....
  7. pmc FOXOs attenuate bone formation by suppressing Wnt signaling
    Srividhya Iyer
    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, USA
    J Clin Invest 123:3409-19. 2013
    ....
  8. pmc The estrogen receptor-alpha in osteoclasts mediates the protective effects of estrogens on cancellous but not cortical bone
    Marta 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...
  9. pmc Estrogen receptor-α signaling in osteoblast progenitors stimulates cortical bone accrual
    Maria 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...
  10. pmc Estrogens attenuate oxidative stress and the differentiation and apoptosis of osteoblasts by DNA-binding-independent actions of the ERalpha
    Maria 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
    ....
  11. pmc Skeletal involution by age-associated oxidative stress and its acceleration by loss of sex steroids
    Maria 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...
  12. ncbi request reprint Proteasomal degradation of Runx2 shortens parathyroid hormone-induced anti-apoptotic signaling in osteoblasts. A putative explanation for why intermittent administration is needed for bone anabolism
    Teresita 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...
  13. pmc PTH receptor signaling in osteocytes governs periosteal bone formation and intracortical remodeling
    Yumie 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...
  14. pmc Targeted deletion of a distant transcriptional enhancer of the receptor activator of nuclear factor-kappaB ligand gene reduces bone remodeling and increases bone mass
    Carlo 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...
  15. pmc Suppression of autophagy in osteocytes mimics skeletal aging
    Melda Onal
    Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
    J Biol Chem 288:17432-40. 2013
    ....
  16. pmc 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 mice
    Melda 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
    ....
  17. pmc Receptor activator of nuclear factor κB ligand (RANKL) protein expression by B lymphocytes contributes to ovariectomy-induced bone loss
    Melda 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...
  18. pmc Continuous elevation of PTH increases the number of osteoblasts via both osteoclast-dependent and -independent mechanisms
    Robert 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...
  19. pmc Osteoprotegerin prevents glucocorticoid-induced osteocyte apoptosis in mice
    Robert 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...
  20. pmc FoxO-mediated defense against oxidative stress in osteoblasts is indispensable for skeletal homeostasis in mice
    Elena 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...
  21. pmc Endogenous glucocorticoids decrease skeletal angiogenesis, vascularity, hydration, and strength in aged mice
    Robert 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
    ....
  22. ncbi request reprint Glucocorticoids act directly on osteoblasts and osteocytes to induce their apoptosis and reduce bone formation and strength
    CHARLES 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...
  23. ncbi request reprint A novel ligand-independent function of the estrogen receptor is essential for osteocyte and osteoblast mechanotransduction
    J 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
    ....
  24. pmc Commitment to the osteoblast lineage is not required for RANKL gene expression
    Carlo 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
    ....
  25. pmc Intermittent PTH stimulates periosteal bone formation by actions on post-mitotic preosteoblasts
    Robert 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...
  26. pmc Basic biology of skeletal aging: role of stress response pathways
    Maria 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
    J Gerontol A Biol Sci Med Sci 68:1197-208. 2013
    ..This article reviews current knowledge on the effects of the aging process on bone, with particular emphasis on the role of ROS and autophagy in cells of the osteoblast lineage in mice. ..
  27. ncbi request reprint Parathyroid hormone stimulates receptor activator of NFkappa B ligand and inhibits osteoprotegerin expression via protein kinase A activation of cAMP-response element-binding protein
    Qiang 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...
  28. pmc FoxO proteins restrain osteoclastogenesis and bone resorption by attenuating H2O2 accumulation
    Shoshana M Bartell
    1 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, USA 2
    Nat Commun 5:3773. 2014
    ....
  29. ncbi request reprint Osteocyte-derived RANKL is a critical mediator of the increased bone resorption caused by dietary calcium deficiency
    Jinhu Xiong
    Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Little Rock, AR, USA Central Arkansas Veterans Healthcare System, Little Rock, AR, USA
    Bone 66:146-54. 2014
    ....
  30. ncbi request reprint Oxidative stress antagonizes Wnt signaling in osteoblast precursors by diverting beta-catenin from T cell factor- to forkhead box O-mediated transcription
    Maria 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
    ....
  31. pmc Dysapoptosis of osteoblasts and osteocytes increases cancellous bone formation but exaggerates cortical porosity with age
    Robert 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, USA
    J Bone Miner Res 29:103-17. 2014
    ..In addition, our findings suggest that distress signals produced by old and/or dysfunctional osteocytes are the culprits of the increased intracortical porosity in old age...
  32. pmc The role of estrogen and androgen receptors in bone health and disease
    Stavros C Manolagas
    Division of Endocrinology and Metabolism, Centre for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences and the Central Arkansas Veterans Healthcare System, 4301 West Markham, Little Rock, AR 72205 7199, USA
    Nat Rev Endocrinol 9:699-712. 2013
    ....
  33. pmc Osteocyte RANKL: new insights into the control of bone remodeling
    Jinhu 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 Grants12

  1. IN VIVO REGULATION OF IL6 AND IL6R GENE EXPRESSION
    CHARLES O BRIEN; Fiscal Year: 1999
    ..Finally, cis-acting regulatory elements in the IL-6 promoter that are the targets for estrogen and PTH actions in vivo will be identified. ..
  2. MOLECULAR CONTROL OF RANKL GENE EXPRESSION
    CHARLES 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. ..
  3. MOLECULAR CONTROL OF RANKL GENE EXPRESSION
    CHARLES O BRIEN; Fiscal Year: 2005
    ..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. ..
  4. MOLECULAR CONTROL OF RANKL GENE EXPRESSION
    CHARLES O BRIEN; Fiscal Year: 2004
    ..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. ..
  5. MOLECULAR CONTROL OF RANKL GENE EXPRESSION
    CHARLES O BRIEN; Fiscal Year: 2003
    ..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. ..
  6. IN VIVO REGULATION OF IL6 AND IL6R GENE EXPRESSION
    CHARLES 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. ..
  7. IN VIVO REGULATION OF IL6 AND IL6R GENE EXPRESSION
    CHARLES O BRIEN; Fiscal Year: 2001
    ..Finally, cis-acting regulatory elements in the IL-6 promoter that are the targets for estrogen and PTH actions in vivo will be identified. ..
  8. MOLECULAR CONTROL OF RANKL GENE EXPRESSION
    CHARLES A O apos BRIEN; Fiscal Year: 2010
    ....
  9. MOLECULAR CONTROL OF RANKL GENE EXPRESSION
    CHARLES O BRIEN; Fiscal Year: 2006
    ..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. ..
  10. IN VIVO REGULATION OF IL6 AND IL6R GENE EXPRESSION
    CHARLES O BRIEN; Fiscal Year: 2000
    ..Finally, cis-acting regulatory elements in the IL-6 promoter that are the targets for estrogen and PTH actions in vivo will be identified. ..
  11. MOLECULAR CONTROL OF RANKL GENE EXPRESSION
    CHARLES O BRIEN; Fiscal Year: 2009
    ....