PMID- 20698779
OWN - NLM
STAT- MEDLINE
DCOM- 20101116
LR  - 20181201
IS  - 2152-4998 (Electronic)
IS  - 2152-4971 (Linking)
VI  - 12
IP  - 4
DP  - 2010 Aug
TI  - CXCR4+ progenitors derived from bone mesenchymal stem cells differentiate into 
      endothelial cells capable of vascular repair after arterial injury.
PG  - 405-15
LID - 10.1089/cell.2009.0088 [doi]
AB  - Recent findings indicate that bone marrow mesenchymal stem cells (BMSCs) 
      participate in the process of neovascularization in response to repair to injury 
      and are involved in postinfarction myocardial repair. It is unclear what special 
      characteristics the vascular progenitors of bone marrow origin has. CXCR4(+) 
      stem/progenitor cells mobilized to the infarct area and improved the myocardial 
      repair. In present study, we aimed to determine whether CXCR4(+)BMSCs contribute 
      to the angiogenic capacity in vitro and in vivo. CXCR4(+)BMSCs were separated by 
      using paramagnetic microbeads and cultured. RT-PCR and FACS analysis confirmed 
      the gene expression phenotype. The uptake of acetylated low density lipoprotein 
      (acLDL) and the tube formation evaluated the function of CXCR4(+)BMSCs. The 
      effect of CXCR4(+)BMSCs transplantation on neovascularization was investigated in 
      a murine model hindlimb ischemia. After induced by VEGF, CXCR4(+)BMSCs expressed 
      the endothelial cells (ECs) phenotype. The expression of EC markers, PECAM-1, and 
      von Willebrand factor (vWF) increased significantly at both the mRNA and protein 
      levels. In addition, CXCR4(+)BMSCs enhanced the uptakes of Dil-acLDL and form 
      capillary-like tubes in vitro. In vivo the local transfer of CXCR4(+)BMSCs 
      increased neovascularization in ischemic hindlimb. These results demonstrate that 
      CXCR4(+)BMSCs differentiate into ECs and contribute to neovascularization in the 
      vascular lesion,, which indicate the important therapeutic implications for 
      cardiovascular diseases and a new cell source for cell-based vascular engineering 
      and repair in the future.
FAU - Li, Mincai
AU  - Li M
AD  - Institute of Pathology, Tongji Hospital, Tongji Medical College, Huazhong 
      University of Science and Technology, Wuhan, People's Republic of China.
FAU - Yu, Jun
AU  - Yu J
FAU - Li, Yan
AU  - Li Y
FAU - Li, Dujuan
AU  - Li D
FAU - Yan, Dan
AU  - Yan D
FAU - Ruan, Qiurong
AU  - Ruan Q
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Cell Reprogram
JT  - Cellular reprogramming
JID - 101528176
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, CXCR4)
SB  - IM
MH  - Animals
MH  - Arteries/*injuries/physiopathology
MH  - Blotting, Western
MH  - Bone Marrow Cells/metabolism
MH  - Bone and Bones/*cytology/metabolism
MH  - Cell Adhesion
MH  - *Cell Differentiation
MH  - Cell Proliferation
MH  - Cells, Cultured
MH  - Endothelium, Vascular/*cytology/physiology
MH  - Female
MH  - Flow Cytometry
MH  - Hindlimb/metabolism/pathology
MH  - Ischemia/metabolism/pathology/*prevention & control
MH  - Mesenchymal Stem Cells/*metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Neovascularization, Physiologic
MH  - RNA, Messenger/genetics
MH  - Receptors, CXCR4/*metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Stem Cells/metabolism
MH  - Wound Healing/physiology
EDAT- 2010/08/12 06:00
MHDA- 2010/11/17 06:00
CRDT- 2010/08/12 06:00
PHST- 2010/08/12 06:00 [entrez]
PHST- 2010/08/12 06:00 [pubmed]
PHST- 2010/11/17 06:00 [medline]
AID - 10.1089/cell.2009.0088 [doi]
PST - ppublish
SO  - Cell Reprogram. 2010 Aug;12(4):405-15. doi: 10.1089/cell.2009.0088.