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P-selectin glycoprotein ligand-1 contributes to wound healing predominantly as a p-selectin ligand and partly as an e-selectin ligand.


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Title: P-selectin glycoprotein ligand-1 contributes to wound healing predominantly as a p-selectin ligand and partly as an e-selectin ligand.
Authors: Tomita, Hajime / Iwata, Yohei / Ogawa, Fumihide / Komura, Kazuhiro / Shimizu, Kazuhiro / Yoshizaki, Ayumi / Hara, Toshihide / Muroi, Eiji / Yanaba, Koichi / Bae, Sangjae / Takenaka, Motoi / Hasegawa, Minoru / Fujimoto, Manabu / Sato, Shinichi
Issue Date: Aug-2009
Publisher: Nature Publishing Group
Citation: Journal of Investigative Dermatology, 129(8), pp.2059-2067; 2009
Abstract: Cell adhesion molecules are critical to wound healing through leukocyte recruitment. Although P-selectin glycoprotein ligand-1 (PSGL-1) regulates leukocyte rolling by binding P-selectin, but also binding E- and L-selectins with lower affinity, little is known about a role of PSGL-1 in wound healing. To clarify a role of PSGL-1 and its interaction with E- and P-selectins in wound healing, we investigated cutaneous wound healing in PSGL-1-deficient (PSGL-1(-/-)) mice in comparison with E-selectin(-/-), P-selectin(-/-), and P-selectin(-/-) mice treated with an anti-E-selectin antibody. PSGL-1 deficiency inhibited early wound healing, which was accompanied by decreased inflammatory cell infiltration and growth factor expression. By contrast, E-selectin deficiency did not affect wound healing. In general, the inhibitory effect of PSGL-1 deficiency on wound healing was similar to that of P-selectin deficiency either alone or with E-selectin blockade. However, early granulation tissue formation, late angiogenesis, and early infiltration of neutrophils and macrophages in PSGL-1(-/-) mice were inhibited beyond the inhibition in P-selectin(-/-) mice, but to a similar level of inhibition in P-selectin(-/-) mice with E-selectin blockade. These results suggest that PSGL-1 contributes to wound healing predominantly as a P-selectin ligand and partly as an E-selectin ligand by mediating infiltration of inflammatory cells.
URI: http://hdl.handle.net/10069/23059
ISSN: 0022202X
DOI: 10.1038/jid.2008.446
PubMed ID: 19177138
Relational Links: http://hdl.handle.net/10069/26714
Rights: © 2009 The Society for Investigative Dermatology
Type: Journal Article
Text Version: author
Appears in Collections:Articles in academic journal

Citable URI : http://hdl.handle.net/10069/23059

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