| First Author | Nagaoka T | Year | 2000 |
| Journal | Am J Pathol | Volume | 157 |
| Issue | 1 | Pages | 237-47 |
| PubMed ID | 10880393 | Mgi Jnum | J:63135 |
| Mgi Id | MGI:1860528 | Doi | 10.1016/S0002-9440(10)64534-8 |
| Citation | Nagaoka T, et al. (2000) Delayed wound healing in the absence of intercellular adhesion molecule-1 or L-selectin expression. Am J Pathol 157(1):237-47 |
| abstractText | Inflammatory cells play a crucial role in wound healing, but the role of adhesion molecules including L-selectin and intercellular adhesion molecule-1 (ICAM-1) is not known in this process. We examined skin wound repair of excisional wounds in mice lacking L-selectin, ICAM-1, or both. The loss of ICAM-1 inhibited wound healing, keratinocyte migration from the edges of the wound toward the center, and granulation tissue formation. By contrast, L-selectin deficiency alone did not affect any of these parameters. However, the loss of both L-selectin and ICAM-1 resulted in inhibition of keratinocyte migration and granulation tissue formation beyond those caused by loss of ICAM-1 alone. Treatment of platelet-derived growth factor to the wounds normalized delayed wound healing in ICAM-1(-/-) mice, but not in L-selectin/ICAM-1(-/-) mice. Therefore, although ICAM-1 contributes to wound repair to a greater extent than L-selectin, a role for L-selectin was revealed in the absence of ICAM-1. The impaired wound repair was associated with reduced infiltration of neutrophils and macrophages in ICAM-1(-/-) and L-selectin/ICAM-1(-/-) mice. These results demonstrate a distinct role of ICAM-1 and L-selectin in wound healing and that the delayed wound healing in the absence of these molecules is likely because of decreased leukocyte accumulation into the wound site. |
