PMID- 22293445
OWN - NLM
STAT- MEDLINE
DCOM- 20120625
LR  - 20190819
IS  - 1347-4820 (Electronic)
IS  - 1346-9843 (Linking)
VI  - 76
IP  - 4
DP  - 2012
TI  - Hypoxic preconditioning enhances angiogenic potential of bone marrow cells with 
      aging-related functional impairment.
PG  - 986-94
AB  - BACKGROUND: Hypoxic preconditioning of bone marrow cells (BMCs) from young 
      healthy individuals can enhance the cells' therapeutic potential. Considering 
      that the response to hypoxia may differ according to the quality of the cells, we 
      assessed the effect of hypoxic preconditioning on BMCs from aged mice and 
      compared the difference in response between BMCs from aged and young mice. 
      METHODS AND RESULTS: BMCs from young (3 months) and aged (20-22 months) mice were 
      subjected to hypoxic preconditioning by culture for 24 h in 2% O(2). Compared with 
      BMCs from young mice, those from aged mice showed significantly fewer CD34- or 
      c-kit-positive stem cells, higher expression of p53, and lower telomerase 
      activity. Adhesion, survival and angiogenic potency were also lower in BMCs from 
      aged mice, indicating an aging-related impairment. Hypoxia-preconditioned BMCs 
      from aged mice showed enhanced adhesion, survival, and angiogenic potency with 
      the in vitro assessments, as well as the in vivo implantation into ischemic 
      hindlimbs. All the enhancements by hypoxic preconditioning were comparable 
      between BMCs from aged and young mice, although the angiogenic potential of BMCs 
      with and without hypoxic preconditioning was lower in old mice compared with 
      young mice. CONCLUSIONS: Similar responses to hypoxia by BMCs from both aged and 
      young mice suggest that hypoxic preconditioning could be a useful method of 
      enhancing the angiogenic potential of BMCs.
FAU - Kubo, Masayuki
AU  - Kubo M
AD  - Department of Surgery and Clinical Science, Yamaguchi University Graduate School 
      of Medicine, Yamaguchi, Japan.
FAU - Li, Tao-Sheng
AU  - Li TS
FAU - Kurazumi, Hiroshi
AU  - Kurazumi H
FAU - Takemoto, Yoshihiro
AU  - Takemoto Y
FAU - Ohshima, Mako
AU  - Ohshima M
FAU - Murata, Tomoaki
AU  - Murata T
FAU - Katsura, Shunsaku
AU  - Katsura S
FAU - Morikage, Noriyasu
AU  - Morikage N
FAU - Furutani, Akira
AU  - Furutani A
FAU - Hamano, Kimikazu
AU  - Hamano K
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120201
PL  - Japan
TA  - Circ J
JT  - Circulation journal : official journal of the Japanese Circulation Society
JID - 101137683
RN  - 0 (Antigens, CD34)
RN  - 0 (Tumor Suppressor Protein p53)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 0 (vascular endothelial growth factor A, mouse)
RN  - EC 2.7.10.1 (Proto-Oncogene Proteins c-kit)
RN  - EC 2.7.7.49 (Telomerase)
SB  - IM
CIN - Circ J. 2012;76(4):823-4. PMID: 22361921
MH  - Age Factors
MH  - Aging/*metabolism
MH  - Animals
MH  - Antigens, CD34/metabolism
MH  - Bone Marrow Cells/*metabolism
MH  - Bone Marrow Transplantation
MH  - Cell Adhesion
MH  - Cell Hypoxia
MH  - Cell Survival
MH  - Cells, Cultured
MH  - Disease Models, Animal
MH  - Endothelial Cells/*metabolism/transplantation
MH  - Hindlimb
MH  - Ischemia/metabolism/physiopathology/surgery
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Muscle, Skeletal/blood supply
MH  - *Neovascularization, Physiologic
MH  - Oxidative Stress
MH  - Proto-Oncogene Proteins c-kit/metabolism
MH  - Telomerase/metabolism
MH  - Tumor Suppressor Protein p53/metabolism
MH  - Vascular Endothelial Growth Factor A/metabolism
EDAT- 2012/02/02 06:00
MHDA- 2012/06/26 06:00
CRDT- 2012/02/02 06:00
PHST- 2012/02/02 06:00 [entrez]
PHST- 2012/02/02 06:00 [pubmed]
PHST- 2012/06/26 06:00 [medline]
AID - JST.JSTAGE/circj/CJ-11-0605 [pii]
AID - 10.1253/circj.cj-11-0605 [doi]
PST - ppublish
SO  - Circ J. 2012;76(4):986-94. doi: 10.1253/circj.cj-11-0605. Epub 2012 Feb 1.