Tetrapeptide AcSDKP Induces Postischemic Neovascularization Through Monocyte Chemoattractant Protein-1 Signaling

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 i...

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Veröffentlicht in:Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 2006-04, Vol.26 (4), p.773-779
Hauptverfasser: Waeckel, Ludovic, Bignon, Jérôme, Liu, Jian-Miao, Markovits, Delphine, Ebrahimian, Téni G, Vilar, José, Mees, Barend, Blanc-Brude, Olivier, Barateau, Véronique, Le ricousse-Roussanne, Sophie, Duriez, Micheline, Tobelem, Gérard, Wdzieczak-Bakala, Joanna, Lévy, Bernard I, Silvestre, Jean-Sébastien
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Sprache:eng
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Zusammenfassung: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
ISSN:1079-5642
1524-4636
DOI:10.1161/01.ATV.0000203510.96492.14