Cell and Tissue Research

, Volume 357, Issue 1, pp 185–194 | Cite as

Impaired mitochondrial function and reduced viability in bone marrow cells of obese mice

  • Genilza Pereira de Oliveira
  • Erika Cortez
  • Graça Justo Araujo
  • Katia Costa de Carvalho Sabino
  • Fabiana Alves Neves
  • Amélia Faustino Bernardo
  • Simone Nunes de Carvalho
  • Anibal Sanchez Moura
  • Laís Carvalho
  • Alessandra Alves Thole
Regular Article

Abstract

Bone marrow cells (BMCs) are the main type of cells used for transplantation therapies. Obesity, a major world health problem, has been demonstrated to affect various tissues, including bone marrow. This could compromise the success of such therapies. One of the main mechanisms underlying the pathogenesis of obesity is mitochondrial dysfunction, and recent data have suggested an important role for mitochondrial metabolism in the regulation of stem cell proliferation and differentiation. Since the potential use of BMCs for clinical therapies depends on their viability and capacity to proliferate and/or differentiate properly, the analysis of mitochondrial function and cell viability could be important approaches for evaluating BMC quality in the context of obesity. We therefore compared BMCs from a control group (CG) and an obese group (OG) of mice and evaluated their mitochondrial function, proliferation capacity, apoptosis, and levels of proteins involved in energy metabolism. BMCs from OG had increased apoptosis and decreased proliferation rates compared with CG. Mitochondrial respiratory capacity, biogenesis, and the coupling between oxidative phosphorylation and ATP synthesis were significantly decreased in OG compared with CG, in correlation with increased levels of uncoupling protein 2 and reduced peroxisome proliferator-activated receptor-coactivator 1α content. OG also had decreased amounts of the glucose transporter GLUT-1 and insulin receptor (IRβ). Thus, Western-diet-induced obesity leads to mitochondrial dysfunction and reduced proliferative capacity in BMCs, changes that, in turn, might compromise the success of therapies utilizing these cells.

Keywords

Bone marrow cells High-fat diet Mitochondria Obesity Oxidative phosphorylation 

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Copyright information

© Springer-Verlag Berlin Heidelberg 2014

Authors and Affiliations

  • Genilza Pereira de Oliveira
    • 1
  • Erika Cortez
    • 1
    • 2
  • Graça Justo Araujo
    • 3
  • Katia Costa de Carvalho Sabino
    • 3
  • Fabiana Alves Neves
    • 2
  • Amélia Faustino Bernardo
    • 2
  • Simone Nunes de Carvalho
    • 1
  • Anibal Sanchez Moura
    • 2
  • Laís Carvalho
    • 1
  • Alessandra Alves Thole
    • 1
  1. 1.Laboratory of Cell Culture, Department of Histology and Embryology, Institute of BiologyState University of Rio de JaneiroRio de JaneiroBrazil
  2. 2.Laboratory of Physiology of Nutrition and Development, Department of Physiological Sciences, Institute of BiologyState University of Rio de JaneiroRio de JaneiroBrazil
  3. 3.Laboratory of Applied Immunology and Biochemistry of Proteins and Natural Products, Department of Biochemistry, Institute of BiologyState University of Rio de JaneiroRio de JaneiroBrazil

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