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PTHrP-Derived Peptides Restore Bone Mass and Strength in Diabetic Mice: Additive Effect of Mechanical Loading.
Maycas, Marta; McAndrews, Kevin A; Sato, Amy Y; Pellegrini, Gretel G; Brown, Drew M; Allen, Matthew R; Plotkin, Lilian I; Gortazar, Arancha R; Esbrit, Pedro; Bellido, Teresita.
Afiliación
  • Maycas M; Department of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
  • McAndrews KA; Instituto de Investigación Sanitaria-Fundación Jiménez Díaz, Madrid, Spain.
  • Sato AY; Department of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
  • Pellegrini GG; Roudebush Veterans Administration Medical Center, Indianapolis, IN, USA.
  • Brown DM; Department of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
  • Allen MR; Department of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
  • Plotkin LI; Department of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
  • Gortazar AR; Department of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
  • Esbrit P; Department of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
  • Bellido T; Roudebush Veterans Administration Medical Center, Indianapolis, IN, USA.
J Bone Miner Res ; 32(3): 486-497, 2017 Mar.
Article en En | MEDLINE | ID: mdl-27683064
There is an unmet need to understand the mechanisms underlying skeletal deterioration in diabetes mellitus (DM) and to develop therapeutic approaches to treat bone fragility in diabetic patients. We demonstrate herein that mice with type 1 DM induced by streptozotocin exhibited low bone mass, inferior mechanical and material properties, increased bone resorption, decreased bone formation, increased apoptosis of osteocytes, and increased expression of the osteocyte-derived bone formation inhibitor Sost/sclerostin. Further, short treatment of diabetic mice with parathyroid hormone related protein (PTHrP)-derived peptides corrected these changes to levels undistinguishable from non-diabetic mice. In addition, diabetic mice exhibited reduced bone formation in response to mechanical stimulation, which was corrected by treatment with the PTHrP peptides, and higher prevalence of apoptotic osteocytes, which was reduced by loading or by the PTHrP peptides alone and reversed by a combination of loading and PTHrP peptide treatment. In vitro experiments demonstrated that the PTHrP peptides or mechanical stimulation by fluid flow activated the survival kinases ERKs and induced nuclear translocation of the canonical Wnt signaling mediator ß-catenin, and prevented the increase in osteocytic cell apoptosis induced by high glucose. Thus, PTHrP-derived peptides cross-talk with mechanical signaling pathways to reverse skeletal deterioration induced by DM in mice. These findings suggest a crucial role of osteocytes in the harmful effects of diabetes on bone and raise the possibility of targeting these cells as a novel approach to treat skeletal deterioration in diabetes. Moreover, our study suggests the potential therapeutic efficacy of combined pharmacological and mechanical stimuli to promote bone accrual and maintenance in diabetic subjects. © 2016 American Society for Bone and Mineral Research.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Huesos / Proteína Relacionada con la Hormona Paratiroidea / Diabetes Mellitus Experimental Tipo de estudio: Prognostic_studies / Risk_factors_studies Límite: Animals Idioma: En Revista: J Bone Miner Res Asunto de la revista: METABOLISMO / ORTOPEDIA Año: 2017 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Huesos / Proteína Relacionada con la Hormona Paratiroidea / Diabetes Mellitus Experimental Tipo de estudio: Prognostic_studies / Risk_factors_studies Límite: Animals Idioma: En Revista: J Bone Miner Res Asunto de la revista: METABOLISMO / ORTOPEDIA Año: 2017 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos