PMID- 16410461
OWN - NLM
STAT- MEDLINE
DCOM- 20060714
LR  - 20121115
IS  - 1524-4636 (Electronic)
IS  - 1079-5642 (Linking)
VI  - 26
IP  - 4
DP  - 2006 Apr
TI  - Tetrapeptide AcSDKP induces postischemic neovascularization through monocyte 
      chemoattractant protein-1 signaling.
PG  - 773-9
AB  - BACKGROUND: We investigated the putative proangiogenic activity and molecular 
      pathway(s) of the tetrapeptide acetyl-N-Ser-Asp-Lys-Pro (AcSDKP) in a model of 
      surgically induced hindlimb ischemia. METHODS AND RESULTS: Hindlimb ischemia was 
      induced by femoral artery ligature and an osmotic minipump was implanted 
      subcutaneously to deliver low (0.12 mg/kg per day) or high (1.2 mg/kg per day) 
      doses of AcSDKP, for 7 or 21 days. Angiography scores, arteriole density, 
      capillary number, and foot perfusion were increased at day 21 in the high-dose 
      AcSDKP-treated mice (by 1.9-, 1.8-, 1.3-, and 1.6-fold, respectively) compared 
      with control animals (P<0.05, P<0.01, P<0.01, respectively). AcSDKP treatment for 
      24 hours upregulated the monocyte chemoattractant protein-1 (MCP-1) mRNA and 
      protein levels by 1.5-fold in cultured endothelial cells (P<0.01). In the 
      ischemic hindlimb model, administration of AcSDKP also enhanced MCP-1 mRNA levels 
      by 90-fold in ischemic leg (P<0.001) and MCP-1 plasma levels by 3-fold (P<0.001 
      versus untreated ischemic control mice). MCP-1 levels upregulation were 
      associated with a 2.3-fold increase in the number of Mac3-positive cells in 
      ischemic area of AcSDKP-treated mice (P<0.001 versus untreated animals). 
      Interestingly, AcSDKP-induced monocyte/macrophage infiltration and postischemic 
      neovascularization was fully blunted in MCP-1-deficient animals. CONCLUSIONS: 
      AcSDKP stimulates postischemic neovascularization through activation of a 
      proinflammatory MCP-1-related pathway.
FAU - Waeckel, Ludovic
AU  - Waeckel L
AD  - Cardiovascular Research Center, INSERM U689, Universite Paris 7, Paris, France.
FAU - Bignon, Jerome
AU  - Bignon J
FAU - Liu, Jian-Miao
AU  - Liu JM
FAU - Markovits, Delphine
AU  - Markovits D
FAU - Ebrahimian, Teni G
AU  - Ebrahimian TG
FAU - Vilar, Jose
AU  - Vilar J
FAU - Mees, Barend
AU  - Mees B
FAU - Blanc-Brude, Olivier
AU  - Blanc-Brude O
FAU - Barateau, Veronique
AU  - Barateau V
FAU - Le Ricousse-Roussanne, Sophie
AU  - Le Ricousse-Roussanne S
FAU - Duriez, Micheline
AU  - Duriez M
FAU - Tobelem, Gerard
AU  - Tobelem G
FAU - Wdzieczak-Bakala, Joanna
AU  - Wdzieczak-Bakala J
FAU - Levy, Bernard I
AU  - Levy BI
FAU - Silvestre, Jean-Sebastien
AU  - Silvestre JS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20060112
PL  - United States
TA  - Arterioscler Thromb Vasc Biol
JT  - Arteriosclerosis, thrombosis, and vascular biology
JID - 9505803
RN  - 0 (Chemokine CCL2)
RN  - 0 (Oligopeptides)
RN  - H041538E9P (goralatide)
SB  - IM
MH  - Animals
MH  - Bone Marrow Cells/pathology
MH  - Cell Differentiation
MH  - Cell Line, Transformed
MH  - Chemokine CCL2/deficiency/*physiology
MH  - Endothelium, Vascular/drug effects/pathology
MH  - Femoral Artery/pathology
MH  - Hindlimb/*blood supply
MH  - Ischemia/*drug therapy/physiopathology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Monocytes/pathology
MH  - Neovascularization, Physiologic/*drug effects
MH  - Oligopeptides/*administration & dosage
MH  - Signal Transduction/drug effects
EDAT- 2006/01/18 09:00
MHDA- 2006/07/15 09:00
CRDT- 2006/01/18 09:00
PHST- 2006/01/18 09:00 [pubmed]
PHST- 2006/07/15 09:00 [medline]
PHST- 2006/01/18 09:00 [entrez]
AID - 01.ATV.0000203510.96492.14 [pii]
AID - 10.1161/01.ATV.0000203510.96492.14 [doi]
PST - ppublish
SO  - Arterioscler Thromb Vasc Biol. 2006 Apr;26(4):773-9. doi: 
      10.1161/01.ATV.0000203510.96492.14. Epub 2006 Jan 12.