Laura McCabe

Summary

Affiliation: Michigan State University
Country: USA

Publications

  1. ncbi request reprint Understanding the skeletal pathology of type 1 and 2 diabetes mellitus
    Laura McCabe
    Department of Physiology, Michigan State University, USA
    Crit Rev Eukaryot Gene Expr 21:187-206. 2011
  2. doi request reprint Probiotic use decreases intestinal inflammation and increases bone density in healthy male but not female mice
    Laura R McCabe
    Department of Physiology, Michigan State University, East Lansing, Michigan 48824, USA
    J Cell Physiol 228:1793-8. 2013
  3. pmc Streptozotocin, type I diabetes severity and bone
    Katherine Motyl
    Departments of Physiology and Radiology, Biomedical Imaging Research Center, Michigan State University, 2201 Biomedical Physical Science Bldg, East Lansing, MI 48824 USA
    Biol Proced Online 11:296-315. 2009
  4. ncbi request reprint Understanding the pathology and mechanisms of type I diabetic bone loss
    Laura R McCabe
    Department of Physiology, Biomedical Imaging Research Center, Michigan State University, 2201 Biomedical Physical Science Building, East Lansing, Michigan 48824, USA
    J Cell Biochem 102:1343-57. 2007
  5. ncbi request reprint Bone loss and increased bone adiposity in spontaneous and pharmacologically induced diabetic mice
    Sergiu Botolin
    Michigan State University, Department of Physiology, East Lansing, Michigan 48824, USA
    Endocrinology 148:198-205. 2007
  6. doi request reprint Bone inflammation and altered gene expression with type I diabetes early onset
    Katherine J Motyl
    Department of Physiology, Biomedical Imaging Research Center, Michigan State University, East Lansing, Michigan 48824, USA
    J Cell Physiol 218:575-83. 2009
  7. ncbi request reprint Adrenomedullin increases AP-1 expression in rat mesangial cells via activation of protein kinase-A and p38 MAPK
    Narayanan Parameswaran
    Department of Physiology, Michigan State University, East Lansing, MI 48824, USA
    Cell Physiol Biochem 13:367-74. 2003
  8. ncbi request reprint Type I diabetic bone phenotype is location but not gender dependent
    Lindsay M Martin
    Department of Physiology, Biomedical Imaging Research Center, Michigan State University, 2201 Biomedical Physical Science Bldg, East Lansing, MI 48824, USA
    Histochem Cell Biol 128:125-33. 2007
  9. ncbi request reprint P38 and activating transcription factor-2 involvement in osteoblast osmotic response to elevated extracellular glucose
    Majd Zayzafoon
    Department of Physiology, Michigan State University, East Lansing, Michigan 48824, USA
    J Biol Chem 277:37212-8. 2002
  10. ncbi request reprint Inhibition of PPARgamma prevents type I diabetic bone marrow adiposity but not bone loss
    Sergiu Botolin
    Department of Physiology and Radiology, Michigan State University, Biomedical Imaging Research Center, East Lansing, MI 48824, USA
    J Cell Physiol 209:967-76. 2006

Research Grants

Collaborators

  • ANN V contact SCHWARTZ
  • N Parameswaran
  • Lindsay M Martin
  • Katherine J Motyl
  • Sergiu Botolin
  • Regina Irwin
  • Jianwei Xie
  • Richard C Schwartz
  • Katherine Motyl
  • Laura Harris
  • John N Dentel
  • Robert W Wiseman
  • Melissa J Baumann
  • Christopher Ontiveros
  • Vidhya V Iyer
  • C Ontiveros
  • Majd Zayzafoon
  • Srinivasan Arjun Tekalur
  • Michelle Raetz
  • Tejas Kadakia
  • Vincent B Young
  • Daniel M Appledorn
  • Andrea Amalfitano
  • Patricia Senagore
  • Hua V Lin
  • Samuel G Blanchard
  • Ron Meyer
  • David P Ankrapp
  • Marie Claude Faugere
  • Michael Orth
  • Hartmut Malluche
  • Tejas B Kadakia
  • R W Wiseman

Detail Information

Publications23

  1. ncbi request reprint Understanding the skeletal pathology of type 1 and 2 diabetes mellitus
    Laura McCabe
    Department of Physiology, Michigan State University, USA
    Crit Rev Eukaryot Gene Expr 21:187-206. 2011
    ..Further research to identify molecular pathways in diabetes-associated bone pathology will provide the basis for therapeutic targets/directions to increase treatment options and improve patient health and well-being...
  2. doi request reprint Probiotic use decreases intestinal inflammation and increases bone density in healthy male but not female mice
    Laura R McCabe
    Department of Physiology, Michigan State University, East Lansing, Michigan 48824, USA
    J Cell Physiol 228:1793-8. 2013
    ..reuteri had no effect on bone parameters in female mice. Taken together our studies indicate that femoral and vertebral bone formation increases in response to oral probiotic use, leading to increased trabecular bone volume in male mice...
  3. pmc Streptozotocin, type I diabetes severity and bone
    Katherine Motyl
    Departments of Physiology and Radiology, Biomedical Imaging Research Center, Michigan State University, 2201 Biomedical Physical Science Bldg, East Lansing, MI 48824 USA
    Biol Proced Online 11:296-315. 2009
    ..In summary, the multiple low-dose STZ mouse model exhibits a similar bone phenotype to spontaneous models, has low toxicity, and serves as a useful tool for examining mechanisms of T1 diabetic bone loss...
  4. ncbi request reprint Understanding the pathology and mechanisms of type I diabetic bone loss
    Laura R McCabe
    Department of Physiology, Biomedical Imaging Research Center, Michigan State University, 2201 Biomedical Physical Science Building, East Lansing, Michigan 48824, USA
    J Cell Biochem 102:1343-57. 2007
    ..Optimizing therapies that prevent bone loss or restore bone density will allow T1-diabetic patients to live longer with strong healthy bones...
  5. ncbi request reprint Bone loss and increased bone adiposity in spontaneous and pharmacologically induced diabetic mice
    Sergiu Botolin
    Michigan State University, Department of Physiology, East Lansing, Michigan 48824, USA
    Endocrinology 148:198-205. 2007
    ..Taken together, multiple streptozotocin injection-induced diabetes is a valid model for understanding the acute and chronic pathophysiologic responses to diabetes and their mechanisms in bone...
  6. doi request reprint Bone inflammation and altered gene expression with type I diabetes early onset
    Katherine J Motyl
    Department of Physiology, Biomedical Imaging Research Center, Michigan State University, East Lansing, Michigan 48824, USA
    J Cell Physiol 218:575-83. 2009
    ..However, inhibition of one cytokine, IFN-gamma was not sufficient to prevent the rapid bone phenotype changes...
  7. ncbi request reprint Adrenomedullin increases AP-1 expression in rat mesangial cells via activation of protein kinase-A and p38 MAPK
    Narayanan Parameswaran
    Department of Physiology, Michigan State University, East Lansing, MI 48824, USA
    Cell Physiol Biochem 13:367-74. 2003
    ..These results indicate a likely role for the members of AP-1 family in AM-mediated biological responses in rat mesangial cells and a role for cAMP activation and subsequent activation of p38 MAPK in AM-induced AP-1 activity...
  8. ncbi request reprint Type I diabetic bone phenotype is location but not gender dependent
    Lindsay M Martin
    Department of Physiology, Biomedical Imaging Research Center, Michigan State University, 2201 Biomedical Physical Science Bldg, East Lansing, MI 48824, USA
    Histochem Cell Biol 128:125-33. 2007
    ..Taken together, our findings indicate that TI-diabetic bone loss in mice is not gender, bone location or bone type dependent, while increased marrow adiposity is location dependent...
  9. ncbi request reprint P38 and activating transcription factor-2 involvement in osteoblast osmotic response to elevated extracellular glucose
    Majd Zayzafoon
    Department of Physiology, Michigan State University, East Lansing, Michigan 48824, USA
    J Biol Chem 277:37212-8. 2002
    ..Therefore, we propose that hyperglycemia-induced increases in p38 MAPK activity and ATF-2 phosphorylation contribute to CRE activation and modulation of c-jun and collagen I expression in osteoblasts...
  10. ncbi request reprint Inhibition of PPARgamma prevents type I diabetic bone marrow adiposity but not bone loss
    Sergiu Botolin
    Department of Physiology and Radiology, Michigan State University, Biomedical Imaging Research Center, East Lansing, MI 48824, USA
    J Cell Physiol 209:967-76. 2006
    ....
  11. pmc Increased bone adiposity and peroxisomal proliferator-activated receptor-gamma2 expression in type I diabetic mice
    Sergiu Botolin
    Department of Physiology, Michigan State University, East Lansing, Michigan 48824, USA
    Endocrinology 146:3622-31. 2005
    ..These findings suggest that IDDM contributes to bone loss through changes in marrow composition resulting in decreased mature osteoblasts and increased adipose accumulation...
  12. ncbi request reprint Chronic hyperglycemia modulates osteoblast gene expression through osmotic and non-osmotic pathways
    Sergiu Botolin
    Molecular Imaging Research Center, 2201 Biomedical Physical Science Building, Department of Physiology, Michigan State University, East Lansing, Michigan 48824, USA
    J Cell Biochem 99:411-24. 2006
    ....
  13. ncbi request reprint Adsorption of serum fetuin to hydroxylapatite does not contribute to osteoblast phenotype modifications
    Jianwei Xie
    Molecular Imaging Research Center, Department of Physiology and Radiology, Michigan State University, 2201 Biomedical Physical Science Building, East Lansing, Michigan, USA
    J Biomed Mater Res A 73:39-47. 2005
    ..This finding suggests that factors intrinsic to HA are required for the response...
  14. ncbi request reprint Simulated microgravity suppresses osteoblast phenotype, Runx2 levels and AP-1 transactivation
    C Ontiveros
    Department of Physiology, Michigan State University, 2201 Biomedical Physical Science Bldg, East Lansing 48824, USA
    J Cell Biochem 88:427-37. 2003
    ..Taken together, our results indicate that simulated microgravity may suppress osteoblast differentiation through decreased runx2 and AP-1 activities...
  15. pmc Leptin treatment prevents type I diabetic marrow adiposity but not bone loss in mice
    Katherine J Motyl
    Department of Physiology, Biomedical Imaging Research Center, Michigan State University, East Lansing, Michigan, USA
    J Cell Physiol 218:376-84. 2009
    ..In summary, we have demonstrated a link between low leptin levels in T1-diabetes and marrow adiposity. However, leptin treatment alone was not successful in preventing bone loss...
  16. doi request reprint Inflammatory bowel disease causes reversible suppression of osteoblast and chondrocyte function in mice
    Laura Harris
    Department of Physiology, Michigan State University, East Lansing, Michigan, USA
    Am J Physiol Gastrointest Liver Physiol 296:G1020-9. 2009
    ..Changes in serum TNF-alpha (increased) and IGF-I (decreased) paralleled changes in bone parameters and returned to normal values with recovery, suggesting a potential role in the skeletal response...
  17. pmc CCAAT/enhancer binding protein β-deficiency enhances type 1 diabetic bone phenotype by increasing marrow adiposity and bone resorption
    Katherine J Motyl
    Department of Biomedical and Integrative Physiology, Biomedical Imaging Research Center, Michigan State University, East Lansing, MI 48824, USA
    Am J Physiol Regul Integr Comp Physiol 300:R1250-60. 2011
    ..02). We conclude that C/EBPβ alone is not responsible for the bone vs. fat phenotype switch observed in T1 diabetes and that suppression of CEBPβ levels may further bone loss and decrease bone stiffness by increasing bone resorption...
  18. pmc Bone and glucose metabolism: a two-way street
    Katherine J Motyl
    Department of Physiology, Michigan State University, East Lansing, MI 48824, USA
    Arch Biochem Biophys 503:2-10. 2010
    ..Further exploration into the physiological and mechanistic effects of ucOC and OC, in rodent models and clinical studies, is necessary to determine to what extent the skeleton regulates energy metabolism in humans...
  19. ncbi request reprint CCAAT/enhancer-binding protein-beta has a role in osteoblast proliferation and differentiation
    Vidhya V Iyer
    Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, MI 48824, USA
    Exp Cell Res 295:128-37. 2004
    ..Thus, C/EBPbeta LAP not only appears to participate in the regulation of genes associated with mature bone physiology, but is also a critical regulator of osteoblast growth and differentiation...
  20. ncbi request reprint Hypoxia suppresses runx2 independent of modeled microgravity
    Christopher Ontiveros
    Molecular Imaging Research Center, Departments of Physiology and Radiology, Michigan State University, East Lansing, Michigan 48824, USA
    J Cell Physiol 200:169-76. 2004
    ..Taken together, our findings indicate that hypoxia associated with skeletal unloading could be major suppressor of runx2 expression leading to suppressed osteoblast differentiation and bone formation...
  21. ncbi request reprint Osteoblasts respond to hydroxyapatite surfaces with immediate changes in gene expression
    Jianwei Xie
    Department of Physiology, Michigan State University, 2201 Biomedical Physical Science Building, East Lansing, Michigan, USA
    J Biomed Mater Res A 71:108-17. 2004
    ..Taken together, we identified HA responsive genes evident within 24 h of surface contact, indicating a critical role for extracellular mineral surfaces in the regulation of osteoblast gene expression and phenotype...
  22. ncbi request reprint Normal bone density obtained in the absence of insulin receptor expression in bone
    Regina Irwin
    Michigan State University, Department of Physiology, 2201 Biomedical Physical Science Building, East Lansing, Michigan 48824, USA
    Endocrinology 147:5760-7. 2006
    ..Taken together, these results suggest that reduced insulin receptor signaling in bone is not a major factor contributing to bone loss in type I diabetes...
  23. ncbi request reprint Inhibition of cross-bridge formation has no effect on contraction-associated phosphorylation of p38 MAPK in mouse skeletal muscle
    John N Dentel
    Molecular Imaging Research Center, Dept of Physiology, Michigan State Univ, 2201 Biomedical and Physical Sciences Bldg, East Lansing, MI 48824, USA
    Am J Physiol Cell Physiol 288:C824-30. 2005
    ..These data do not support the view that force generation per se activates p38 MAPK and suggest that other events associated with contraction must be responsible...

Research Grants6

  1. Diabetic/osmotic Influences on Osteoblast Phenotype
    Laura McCabe; Fiscal Year: 2007
    ..Our results will suggest targets for ameliorating the effects of type I diabetes on bone. ..