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(Journal of Leukocyte Biology. 2006;79:971-976.)
© 2006 by Society for Leukocyte Biology

Ischemia-induced angiogenesis: role of inflammatory response mediated by P-selectin

Kimiyasu Egami*, Toyoaki Murohara{dagger},1, Mika Aoki{dagger} and Toyojiro Matsuishi*

* Department of Pediatrics, Kurume University School of Medicine, Japan; and
{dagger} Department of Cardiology, Nagoya University Graduate School of Medicine, Japan

1Correspondence: Department of Cardiology, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa-ku, Nagoya 466-8550 Japan. E-mail: murohara{at}med.nagoya-u.ac.jp

ABSTRACT

P-selectin is a 140-kDa glycoprotein expressed on endothelial cells and platelets. P-selectin mediates the tethering and rolling of leukocytes along the endothelium, an early step of leukocyte extravasation. Although inflammation is a requisite process for ischemia-induced angiogenesis, little is known regarding the role of P-selectin in angiogenesis in the setting of tissue ischemia. We examined whether ischemia-induced angiogenesis is altered in P-selectin knockout (P-selectin–/–) mice. Angiogenesis was evaluated in a surgically induced hind-limb ischemia model using laser Doppler blood flowmetry (LDBF) and histological capillary density (CD). After left hind-limb ischemia, the ischemic/normal limb LDBF ratio was persistently lower in P-selectin–/– mice compared with wild-type (WT) mice. CD was also significantly lower in P-selectin–/– mice than in WT mice on Postoperative Day 14. Fewer numbers of total CD45+ inflammatory leukocytes infiltrated into the ischemic tissues in P-selectin–/– mice than in WT mice, and immunohistochemical analysis revealed the number of infiltrated leukocytes expressing vascular endothelial growth factor was also decreased in P-selectin–/– mice. P-selectin mRNA expression was augmented after hind-limb ischemia in WT mice. In conclusion, P-selectin may play an important role in ischemia-induced angiogenesis by promoting early inflammatory mononuclear cell infiltration. P-selectin would become one possible target molecule for modulating inflammatory angiogenesis.

Key Words: peripheral circulation • growth factor • animal model • human disease




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