PMID- 24744266
OWN - NLM
STAT- MEDLINE
DCOM- 20150417
LR  - 20140701
IS  - 1432-0878 (Electronic)
IS  - 0302-766X (Linking)
VI  - 357
IP  - 1
DP  - 2014 Jul
TI  - Impaired mitochondrial function and reduced viability in bone marrow cells of 
      obese mice.
PG  - 185-94
LID - 10.1007/s00441-014-1857-1 [doi]
AB  - 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 1alpha content. OG also had 
      decreased amounts of the glucose transporter GLUT-1 and insulin receptor (IRbeta). 
      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.
FAU - de Oliveira, Genilza Pereira
AU  - de Oliveira GP
AD  - Laboratory of Cell Culture, Department of Histology and Embryology, Institute of 
      Biology, State University of Rio de Janeiro, Av. Professor Manoel de Abreu 444, 
      Rio de Janeiro, Brazil.
FAU - Cortez, Erika
AU  - Cortez E
FAU - Araujo, Graca Justo
AU  - Araujo GJ
FAU - de Carvalho Sabino, Katia Costa
AU  - de Carvalho Sabino KC
FAU - Neves, Fabiana Alves
AU  - Neves FA
FAU - Bernardo, Amelia Faustino
AU  - Bernardo AF
FAU - de Carvalho, Simone Nunes
AU  - de Carvalho SN
FAU - Moura, Anibal Sanchez
AU  - Moura AS
FAU - Carvalho, Lais
AU  - Carvalho L
FAU - Thole, Alessandra Alves
AU  - Thole AA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140418
PL  - Germany
TA  - Cell Tissue Res
JT  - Cell and tissue research
JID - 0417625
SB  - IM
MH  - Animals
MH  - Bone Marrow Cells/*cytology/metabolism
MH  - Cell Survival/physiology
MH  - Male
MH  - Mice
MH  - Mice, Obese
MH  - Mitochondria/*physiology
MH  - Obesity/metabolism/*pathology
MH  - Oxidative Phosphorylation
MH  - Signal Transduction
EDAT- 2014/04/20 06:00
MHDA- 2015/04/18 06:00
CRDT- 2014/04/19 06:00
PHST- 2013/08/13 00:00 [received]
PHST- 2014/02/20 00:00 [accepted]
PHST- 2014/04/19 06:00 [entrez]
PHST- 2014/04/20 06:00 [pubmed]
PHST- 2015/04/18 06:00 [medline]
AID - 10.1007/s00441-014-1857-1 [doi]
PST - ppublish
SO  - Cell Tissue Res. 2014 Jul;357(1):185-94. doi: 10.1007/s00441-014-1857-1. Epub 
      2014 Apr 18.