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Disruption of the Cx43/miR21 pathway leads to osteocyte apoptosis and increased osteoclastogenesis with aging.
Davis, Hannah M; Pacheco-Costa, Rafael; Atkinson, Emily G; Brun, Lucas R; Gortazar, Arancha R; Harris, Julia; Hiasa, Masahiro; Bolarinwa, Surajudeen A; Yoneda, Toshiyuki; Ivan, Mircea; Bruzzaniti, Angela; Bellido, Teresita; Plotkin, Lilian I.
Afiliación
  • Davis HM; Department of Anatomy & Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
  • Pacheco-Costa R; Department of Anatomy & Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
  • Atkinson EG; Department of Anatomy & Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
  • Brun LR; Department of Anatomy & Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
  • Gortazar AR; Instituto de Medicina Molecular Aplicada, Facultad de Medicina, Universidad San Pablo-CEU, Madrid, Spain.
  • Harris J; Department of Anatomy & Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
  • Hiasa M; Division of Hematology/Oncology, Department of Internal Medicine, Indiana University School of Medicine, Indianapolis, IN, USA.
  • Bolarinwa SA; Department of Anatomy & Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
  • Yoneda T; Division of Hematology/Oncology, Department of Internal Medicine, Indiana University School of Medicine, Indianapolis, IN, USA.
  • Ivan M; Division of Hematology/Oncology, Department of Internal Medicine, Indiana University School of Medicine, Indianapolis, IN, USA.
  • Bruzzaniti A; Department of Oral Biology, Indiana University School of Dentistry, Indianapolis, IN, USA.
  • Bellido T; Department of Anatomy & Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
  • Plotkin LI; Division of Endocrinology, Department of Internal Medicine, Indiana University School of Medicine, Indianapolis, IN, USA.
Aging Cell ; 16(3): 551-563, 2017 06.
Article en En | MEDLINE | ID: mdl-28317237
Skeletal aging results in apoptosis of osteocytes, cells embedded in bone that control the generation/function of bone forming and resorbing cells. Aging also decreases connexin43 (Cx43) expression in bone; and osteocytic Cx43 deletion partially mimics the skeletal phenotype of old mice. Particularly, aging and Cx43 deletion increase osteocyte apoptosis, and osteoclast number and bone resorption on endocortical bone surfaces. We examined herein the molecular signaling events responsible for osteocyte apoptosis and osteoclast recruitment triggered by aging and Cx43 deficiency. Cx43-silenced MLO-Y4 osteocytic (Cx43def ) cells undergo spontaneous cell death in culture through caspase-3 activation and exhibit increased levels of apoptosis-related genes, and only transfection of Cx43 constructs able to form gap junction channels reverses Cx43def cell death. Cx43def cells and bones from old mice exhibit reduced levels of the pro-survival microRNA miR21 and, consistently, increased levels of the miR21 target phosphatase and tensin homolog (PTEN) and reduced phosphorylated Akt, whereas PTEN inhibition reduces Cx43def cell apoptosis. miR21 reduction is sufficient to induce apoptosis of Cx43-expressing cells and miR21 deletion in miR21fl/fl bones increases apoptosis-related gene expression, whereas a miR21 mimic prevents Cx43def cell apoptosis, demonstrating that miR21 lies downstream of Cx43. Cx43def cells release more osteoclastogenic cytokines [receptor activator of NFκB ligand (RANKL)/high-mobility group box-1 (HMGB1)], and caspase-3 inhibition prevents RANKL/HMGB1 release and the increased osteoclastogenesis induced by conditioned media from Cx43def cells, which is blocked by antagonizing HMGB1-RAGE interaction. These findings identify a novel Cx43/miR21/HMGB1/RANKL pathway involved in preventing osteocyte apoptosis that also controls osteoclast formation/recruitment and is impaired with aging.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Osteoclastos / Osteocitos / Osteogénesis / Envejecimiento / Conexina 43 / MicroARNs Tipo de estudio: Prognostic_studies Idioma: En Revista: Aging Cell Año: 2017 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Osteoclastos / Osteocitos / Osteogénesis / Envejecimiento / Conexina 43 / MicroARNs Tipo de estudio: Prognostic_studies Idioma: En Revista: Aging Cell Año: 2017 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido