ERNESTO M CANALIS

Summary

Affiliation: Saint Francis Hospital and Medical Center
Country: USA

Publications

  1. ncbi Perspectives on glucocorticoid-induced osteoporosis
    Ernesto Canalis
    Saint Francis Hospital and Medical Center, Hartford, CT 06105, USA
    Bone 34:593-8. 2004
  2. ncbi Mechanisms of glucocorticoid action in bone
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, 114 Woodland Street, Hartford, CT 06105 1299, USA
    Curr Osteoporos Rep 3:98-102. 2005
  3. ncbi Signals that determine the fate of osteoblastic cells
    E Canalis
    Department of Research, Saint Francis Hospital and Medical Center 114, Woodland Street, Hartford, CT 06105 1299, USA
    J Endocrinol Invest 28:3-7. 2005
  4. pmc Connective tissue growth factor is a target of notch signaling in cells of the osteoblastic lineage
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, CT, 06105 The University of Connecticut School of Medicine, Farmington, CT, 06030 Electronic address
    Bone 64:273-80. 2014
  5. doi Wnt signalling in osteoporosis: mechanisms and novel therapeutic approaches
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Centre, 114 Woodland Street, Hartford, CT 06105 1299, USA
    Nat Rev Endocrinol 9:575-83. 2013
  6. pmc Notch signaling in osteocytes differentially regulates cancellous and cortical bone remodeling
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, Connecticut 06105 1299, USA
    J Biol Chem 288:25614-25. 2013
  7. pmc Osteoblast lineage-specific effects of notch activation in the skeleton
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, 114 Woodland Street, Hartford, CT 06105 1299, USA
    Endocrinology 154:623-34. 2013
  8. pmc Conditional inactivation of noggin in the postnatal skeleton causes osteopenia
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, 114 Woodland Street, Hartford, CT 06105 1299, USA
    Endocrinology 153:1616-26. 2012
  9. ncbi Bone morphogenetic proteins, their antagonists, and the skeleton
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, Connecticut 06105, USA
    Endocr Rev 24:218-35. 2003
  10. ncbi Mechanisms of glucocorticoid-induced osteoporosis
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, and University of Connecticut School of Medicine, Farmington, Connecticut, USA
    Curr Opin Rheumatol 15:454-7. 2003

Research Grants

  1. Somatomedin: Autologous Regulator of Bone Formation
    Ernesto Canalis; Fiscal Year: 2008

Collaborators

Detail Information

Publications37

  1. ncbi Perspectives on glucocorticoid-induced osteoporosis
    Ernesto Canalis
    Saint Francis Hospital and Medical Center, Hartford, CT 06105, USA
    Bone 34:593-8. 2004
  2. ncbi Mechanisms of glucocorticoid action in bone
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, 114 Woodland Street, Hartford, CT 06105 1299, USA
    Curr Osteoporos Rep 3:98-102. 2005
    ..Glucocorticoids alter the growth hormone/insulin-like growth factor axis in cartilage and, as a consequence, suppress linear growth...
  3. ncbi Signals that determine the fate of osteoblastic cells
    E Canalis
    Department of Research, Saint Francis Hospital and Medical Center 114, Woodland Street, Hartford, CT 06105 1299, USA
    J Endocrinol Invest 28:3-7. 2005
    ..Notch, a family of transmembrane receptors, opposes Wnt signaling and inhibits osteoblastic differentiation. BMP, Wnt and Notch play a central role in osteoblastic cell fate...
  4. pmc Connective tissue growth factor is a target of notch signaling in cells of the osteoblastic lineage
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, CT, 06105 The University of Connecticut School of Medicine, Farmington, CT, 06030 Electronic address
    Bone 64:273-80. 2014
    ..In conclusion, Ctgf is a target of Notch canonical signaling in osteoblasts, and may act in concert with Notch to regulate skeletal homeostasis. ..
  5. doi Wnt signalling in osteoporosis: mechanisms and novel therapeutic approaches
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Centre, 114 Woodland Street, Hartford, CT 06105 1299, USA
    Nat Rev Endocrinol 9:575-83. 2013
    ..Consequently, Wnt signalling can be targeted by the neutralization of its extracellular antagonists to obtain a skeletal anabolic response. ..
  6. pmc Notch signaling in osteocytes differentially regulates cancellous and cortical bone remodeling
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, Connecticut 06105 1299, USA
    J Biol Chem 288:25614-25. 2013
    ..In conclusion, Notch plays a unique role in osteocytes, up-regulates osteoprotegerin and Wnt signaling, and differentially regulates trabecular and cortical bone homeostasis. ..
  7. pmc Osteoblast lineage-specific effects of notch activation in the skeleton
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, 114 Woodland Street, Hartford, CT 06105 1299, USA
    Endocrinology 154:623-34. 2013
    ....
  8. pmc Conditional inactivation of noggin in the postnatal skeleton causes osteopenia
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, 114 Woodland Street, Hartford, CT 06105 1299, USA
    Endocrinology 153:1616-26. 2012
    ..In conclusion, Noggin inactivation causes osteopenia, suggesting that BMP in excess have a detrimental effect on bone or that noggin has a BMP-independent role in skeletal homeostasis...
  9. ncbi Bone morphogenetic proteins, their antagonists, and the skeleton
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, Connecticut 06105, USA
    Endocr Rev 24:218-35. 2003
    ..The antagonists tend to be specific for BMPs and are regulated by BMPs, indicating the existence and need of local feedback mechanisms to temper BMP cellular activities...
  10. ncbi Mechanisms of glucocorticoid-induced osteoporosis
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, and University of Connecticut School of Medicine, Farmington, Connecticut, USA
    Curr Opin Rheumatol 15:454-7. 2003
    ..Eventually, the inhibition of bone formation will cause a decrease in bone remodeling and a continued increased risk of fractures...
  11. doi Notch signaling in osteoblasts
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, 114 Woodland Street, Hartford, CT 06105, USA
    Sci Signal 1:pe17. 2008
    ....
  12. ncbi Nephroblastoma overexpressed (Nov) is a novel bone morphogenetic protein antagonist
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, CT 06105 1299, USA
    Ann N Y Acad Sci 1116:50-8. 2007
    ..GST pulldown experiments demonstrated direct Nov-BMP interactions. In conclusion, Nov has BMP antagonistic properties and inhibits osteoblastogenesis and osteoblastic function...
  13. pmc Growth factor control of bone mass
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, Connecticut 06105 1299, USA
    J Cell Biochem 108:769-77. 2009
    ..Clinical trials are needed to determine the long-term effectiveness and safety of novel anabolic agents for the management of osteoporosis...
  14. pmc Nephroblastoma overexpressed (Nov) inactivation sensitizes osteoblasts to bone morphogenetic protein-2, but nov is dispensable for skeletal homeostasis
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, 114 Woodland Street, Hartford, Connecticut 06105 1299, USA
    Endocrinology 151:221-33. 2010
    ..Surface plasmon resonance demonstrated direct interactions between Nov and BMP-2. In conclusion, Nov sensitizes osteoblasts to BMP-2, but Nov is dispensable for the maintenance of bone mass...
  15. ncbi Effects of glucocorticoids on the skeleton
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, CT 06105 1299, USA
    J Pediatr Endocrinol Metab 15:1341-5. 2002
    ..The most significant actions of glucocorticoids are on chondrocytes and bone-forming cells, where they act, directly and indirectly, and regulate the local synthesis of insulin-like growth factor-I...
  16. pmc New treatment modalities in osteoporosis
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, Connecticut 06105 1299, USA
    Endocr Pract 16:855-63. 2010
    ..To describe recently discovered agents for the management of osteoporosis...
  17. ncbi Mechanisms of glucocorticoid action in bone
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, Connecticut 06105, USA
    Ann N Y Acad Sci 966:73-81. 2002
    ..Bisphosphonates inhibit bone resorption and prevent and revert the bone loss that follows glucocorticoid exposure. Anabolic agents, such as parathyroid hormone, stimulate bone formation and can increase bone mass in GIOP...
  18. pmc Update in new anabolic therapies for osteoporosis
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, Connecticut 06105 1299, USA
    J Clin Endocrinol Metab 95:1496-504. 2010
    ..Clinical trials are being conducted to test the long-term effectiveness and safety of novel bone anabolic agents...
  19. pmc Connective tissue growth factor is required for skeletal development and postnatal skeletal homeostasis in male mice
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, Connecticut 06105 1299, USA
    Endocrinology 151:3490-501. 2010
    ..In conclusion, CTGF is necessary for normal skeletal development but to a lesser extent for postnatal skeletal homeostasis...
  20. pmc Gremlin1 is required for skeletal development and postnatal skeletal homeostasis
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, Connecticut 06105 1299, USA
    J Cell Physiol 227:269-77. 2012
    ....
  21. ncbi Mechanisms of anabolic therapies for osteoporosis
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, CT 06105 1299, USA
    N Engl J Med 357:905-16. 2007
  22. ncbi Parathyroid hormone increases mac25/insulin-like growth factor-binding protein-related protein-1 expression in cultured osteoblasts
    R C Pereira
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, Connecticut 06105 1299, USA
    Endocrinology 140:1998-2003. 1999
    ..In conclusion, PTH stimulates mac25/IGFBP-RP-1 transcription in osteoblasts, an effect that could be relevant to the actions of PTH in bone...
  23. ncbi Dual regulation of stromelysin-3 by fibroblast growth factor-2 in murine osteoblasts
    A M Delany
    Departments of Research and Medicine, Saint Francis Hospital and Medical Center, Hartford, Connecticut 06105, USA
    J Biol Chem 273:16595-600. 1998
    ..This complex regulation may be important in the function of stromelysin-3 in bone and in remodeling processes, such as wound and fracture repair...
  24. ncbi Basic fibroblast growth factor stimulates collagenase-3 promoter activity in osteoblasts through an activator protein-1-binding site
    S Varghese
    Department of Research and Medicine, Saint Francis Hospital and Medical Center, Hartford, Connecticut 06105, USA
    Endocrinology 141:2185-91. 2000
    ..The stimulation of collagenase-3 synthesis by bFGF may be critical in mediating the actions of this growth factor in bone remodeling...
  25. ncbi The metastasis-associated metalloproteinase stromelysin-3 is induced by transforming growth factor-beta in osteoblasts and fibroblasts
    A M Delany
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, Connecticut 06105, USA
    Endocrinology 142:1561-6. 2001
    ..Stimulation of stromelysin-3 expression by TGF-beta in fibroblasts and osteoblasts could play a role in the metastasis of breast cancer cells and their homing and survival in bone...
  26. ncbi Glucocorticoid suppression of IGF I transcription in osteoblasts
    A M Delany
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, Connecticut 06105, USA
    Mol Endocrinol 15:1781-9. 2001
    ..In conclusion, cortisol represses IGF I transcription in osteoblasts, and CAAT/enhancer binding proteins appear to play a role in this effect...
  27. ncbi Transforming growth factor-beta increases interleukin-6 transcripts in osteoblasts
    N Franchimont
    Department of Research and Medicine, Saint Francis Hospital and Medical Center, Hartford, CT, USA
    Bone 26:249-53. 2000
    ..Transforming growth factor-beta upregulation of IL-6 may be critical in conditions of increased bone resorption, such as myeloma...
  28. ncbi Cortisol enhances the expression of mac25/insulin-like growth factor-binding protein-related protein-1 in cultured osteoblasts
    R C Pereira
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, Connecticut 06105, USA
    Endocrinology 140:228-32. 1999
    ..As IGFBP-rP1 binds and possibly modifies the effects of IGFs and insulin, its increased expression could be relevant to the inhibitory actions of cortisol in bone...
  29. pmc Osteopenia and decreased bone formation in osteonectin-deficient mice
    A M Delany
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, Connecticut 06105, USA
    J Clin Invest 105:915-23. 2000
    ..These data indicate that osteonectin supports bone remodeling and the maintenance of bone mass in vertebrates...
  30. ncbi Cortisol inhibits the differentiation and apoptosis of osteoblasts in culture
    R M Pereira
    Department of Research, Saint Francis Hospital and Medical Center, 114 Woodland Street, Hartford, CT 06105-1299, USA
    Bone 28:484-90. 2001
    ....
  31. ncbi Overexpression of insulin-like growth factor binding protein-5 decreases osteoblastic function in vitro
    D Durant
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, CT 06105 1299, USA
    Bone 35:1256-62. 2004
    ..IGFBP-5 caused a modest stimulation of DNA synthesis. In conclusion, overexpression of IGFBP-5 decreases osteoblastic function possibly by binding IGFs in the bone microenvironment...
  32. ncbi Directing the expression of a green fluorescent protein transgene in differentiated osteoblasts: comparison between rat type I collagen and rat osteocalcin promoters
    Z Kalajzic
    Department of Genetics and Developmental Biology, University of Connecticut Health Center, Farmington, Connecticut 06030, USA
    Bone 31:654-60. 2002
    ..The different temporal and spatial pattern of each transgene in vivo and in vitro reveals potential advantages and disadvantages of these two transgene models...
  33. ncbi Transgenic mice overexpressing insulin-like growth factor binding protein-5 display transiently decreased osteoblastic function and osteopenia
    R D Devlin
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, Connecticut 06105 1299, USA
    Endocrinology 143:3955-62. 2002
    ..In conclusion, transgenic mice overexpressing IGFBP-5 in the bone microenvironment have a transient decrease in trabecular bone volume, impaired osteoblastic function, and osteopenia...
  34. ncbi Noggin arrests stromal cell differentiation in vitro
    E Gazzerro
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, CT 06105 1299, USA
    Bone 32:111-9. 2003
    ..In conclusion, noggin arrests the differentiation of stromal cells, preventing cellular maturation...
  35. ncbi Transgenic mice expressing selected insulin-like growth factor-binding protein-5 fragments do not exhibit enhanced bone formation
    D Durant
    Department of Research, Saint Francis Hospital and Medical Center, 114 Woodland St, Hartford, CT 06105 1299, USA
    Growth Horm IGF Res 14:319-27. 2004
    ..In conclusion, transgenic mice expressing IGFBP-5 1-162 and 1-193 in the bone microenvironment do not exhibit an obvious skeletal phenotype...
  36. ncbi Glucocorticoid-induced osteoporosis: pathophysiology and therapy
    E Canalis
    Saint Francis Hospital and Medical Center, Hartford, CT 060105, USA
    Osteoporos Int 18:1319-28. 2007
    ..Glucocorticoids also favor osteoclastogenesis and as a consequence increase bone resorption. Bisphosphonates are effective in the prevention and treatment of GIO. Anabolic therapeutic strategies are under investigation...
  37. pmc Notch and the skeleton
    Stefano Zanotti
    Department of Research, Saint Francis Hospital and Medical Center, 114 Woodland Street, Hartford, CT 06105 1299, USA
    Mol Cell Biol 30:886-96. 2010
    ..Dysregulation of Notch signaling is the underlying cause of diseases affecting the skeletal tissue, including Alagille syndrome, spondylocostal dysostosis, and possibly, osteosarcoma...

Research Grants1

  1. Somatomedin: Autologous Regulator of Bone Formation
    Ernesto Canalis; Fiscal Year: 2008
    ..These investigations should clarify the role of CHOP in bone cell differentiation and function. [unreadable] [unreadable]..