Li C H, Amar S
Department of Periodontology & Oral Biology, Goldman School of Dental Medicine, Boston University, Boston, MA 02118, USA.
J Dent Res. 2006 Apr;85(4):374-8. doi: 10.1177/154405910608500418.
Wound healing is a complex cascade of events, which diminishes the size of the wound and reestablishes tissue integrity. Secreted frizzled-related protein 1 (SFRP1) contributes to the inhibition of apoptosis in fibroblast populations. We investigated the role of SFRP1 in a mouse wound-healing model; 2.0-mm excisional wounds were created in the scalp and hard palate. Healing responses were measured by histomorphometric analysis, apoptosis assay, and immunohistochemistry. Dermal wounds did not harbor SFRP1, but healed faster than palatal wounds which expressed significant levels of SFRP1. Antibody experiments aimed at blocking SFRP1 in palatal wounds resulted in promotion of wound closure, enhancement of new tissue formation, decrease of inflammatory cell infiltrate, and increase of apoptotic fibroblasts. Analysis of the present data suggests that SFRP1 may be partly responsible for the poorer healing performance of the palatal wounds compared with dermal wounds. Blocking SFRP1 results in improvement of palatal healing outcomes.
伤口愈合是一系列复杂的事件,它会减小伤口大小并重新建立组织完整性。分泌型卷曲相关蛋白1(SFRP1)有助于抑制成纤维细胞群体中的细胞凋亡。我们在小鼠伤口愈合模型中研究了SFRP1的作用;在头皮和硬腭上制造2.0毫米的切除伤口。通过组织形态计量分析、细胞凋亡检测和免疫组织化学来测量愈合反应。皮肤伤口中不存在SFRP1,但愈合速度比表达大量SFRP1的腭部伤口更快。旨在阻断腭部伤口中SFRP1的抗体实验导致伤口闭合加速、新组织形成增强、炎性细胞浸润减少以及凋亡成纤维细胞增加。对现有数据的分析表明,与皮肤伤口相比,SFRP1可能是腭部伤口愈合性能较差的部分原因。阻断SFRP1可改善腭部愈合结果。