PMID- 15854667
OWN - NLM
STAT- MEDLINE
DCOM- 20050623
LR  - 20091119
IS  - 0022-4804 (Print)
IS  - 0022-4804 (Linking)
VI  - 125
IP  - 2
DP  - 2005 May 15
TI  - Expression of TGF-beta1 in smooth muscle cells regulates endothelial progenitor 
      cells migration and differentiation.
PG  - 151-6
AB  - OBJECTIVE: Endothelial angiogenesis in the intima of the arterial wall is one of 
      key events in the pathogenesis of arteriosclerosis. The molecular mechanisms by 
      which transforming growth factor beta 1 (TGFbeta1) and endothelial progenitor 
      cells may be responsible for angiogenesis of arteriosclerosis lesions are poorly 
      understood. MATERIALS AND METHODS: Primary culture smooth muscle cells were 
      transfected with pMAMneoTGFbeta1. ELISA checked VEGF expression in smooth muscle 
      cells. Human EPCs (CD34+ cells) were cultured in pMAMneoTGFbeta1 or pMAMneo 
      transfected smooth muscle cells conditional medium. After 21 days, differentiated 
      endothelial colonies were confirmed by immunofluorescence for von Willebrand 
      factor (vWF) and vascular-endothelial (VE)-cadherin. The VEGFR-1 expression in 
      differentiated endothelial colonies was detected by ELISA. Cells migration and 
      adhesion toward pMAMneoTGFbeta1 and pMAMneo transfected smooth muscle cells were 
      also measured in parallel flow chamber. RESULTS: Abundant TGFbeta1 stable 
      expressed in smooth muscle cells. TGFbeta1 transfected smooth muscle cells 
      expressed significantly higher level VEGF than pMAMneo group. As judged by 
      positive staining for endothelial markers vWF and VE-cadherin, the combination of 
      TGFbeta1 transfected smooth muscle cells conditional medium produced 
      significantly more endothelial colonies (P<0.05) than did pMAMneo group. The 
      adhesion force between endothelial progenitor cells and smooth muscle cells in 
      TGFbeta1 group was higher than control. CONCLUSION: TGFbeta1 expressed smooth 
      muscle cells can be helpful for increasing endothelial progenitor cells adhesion 
      and differentiation. It may be responsible for angiogenesis of arteriosclerosis 
      lesions and useful for blood vessel tissue engineering.
FAU - Zhu, Chuhong
AU  - Zhu C
AD  - Department of Anatomy, Biomechanics Section under the Key Lab for Biomechanics & 
      Tissue Engineering of Ministry of Education, Third Military Medical University, 
      Chongqing, China. zhuch99@yahoo.com
FAU - Ying, Dajun
AU  - Ying D
FAU - Zhou, Dinghua
AU  - Zhou D
FAU - Mi, Jianhong
AU  - Mi J
FAU - Zhang, Wei
AU  - Zhang W
FAU - Chang, Qing
AU  - Chang Q
FAU - Li, Li
AU  - Li L
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Surg Res
JT  - The Journal of surgical research
JID - 0376340
RN  - 0 (Antigens, CD)
RN  - 0 (Cadherins)
RN  - 0 (TGFB1 protein, human)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 0 (cadherin 5)
RN  - 0 (von Willebrand Factor)
RN  - EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-1)
SB  - IM
MH  - Antigens, CD
MH  - Arteriosclerosis/metabolism
MH  - Cadherins/metabolism
MH  - Cell Adhesion
MH  - Cell Culture Techniques
MH  - Cell Differentiation
MH  - Endothelial Cells/*metabolism
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Humans
MH  - Muscle, Smooth, Vascular/*metabolism/physiopathology
MH  - Neovascularization, Pathologic/metabolism
MH  - Stem Cells/*metabolism
MH  - Transforming Growth Factor beta/*metabolism
MH  - Transforming Growth Factor beta1
MH  - Vascular Endothelial Growth Factor A/metabolism
MH  - Vascular Endothelial Growth Factor Receptor-1/metabolism
MH  - von Willebrand Factor/metabolism
EDAT- 2005/04/28 09:00
MHDA- 2005/06/24 09:00
CRDT- 2005/04/28 09:00
PHST- 2004/07/18 00:00 [received]
PHST- 2004/12/09 00:00 [revised]
PHST- 2004/12/11 00:00 [accepted]
PHST- 2005/04/28 09:00 [pubmed]
PHST- 2005/06/24 09:00 [medline]
PHST- 2005/04/28 09:00 [entrez]
AID - S0022-4804(04)00711-5 [pii]
AID - 10.1016/j.jss.2004.12.006 [doi]
PST - ppublish
SO  - J Surg Res. 2005 May 15;125(2):151-6. doi: 10.1016/j.jss.2004.12.006.