生物谷报道：英国布里斯托尔大学（University of Bristol）的一项研究表明，抑制一个基因就能使伤口愈合较快，并减少疤痕。这个发现重大的意义，不仅对皮肤伤口，而且对患病或腹部手术所造成的器官组织损伤都有重大意义。
当皮肤受损血块形成时，伤口底下的细胞开始修复损伤，导致疤痕的出现。疤痕是组织修复过程中自然出现的，在割伤或烧伤后的皮肤非常显眼。疤痕可能很小，如膝盖擦伤；也可能很大，如糖尿病腿部溃疡。而且疤痕也不仅限于皮肤。所有的组织修复是都会产生疤痕，比如说，酒精性肝损伤会导致纤维化和肝功能衰竭；腹部手术后的疤痕常可导致严重并发症发生。
组织损伤会诱发炎症反应，释放白色细胞杀死微生物，以保护皮肤免受感染。同样是白色细胞引导胶原蛋白层的生成，而这些胶原蛋白层帮助伤口愈合，但它们从周围的皮肤突出来，并造成疤痕。布里斯托尔大学的Paul Martin教授及其同事的研究结果表明，骨桥蛋白（osteopontin，OPN）是触发疤痕形成的基因之一。在伤口敷上一种能够抑制OPN的胶体，可以加速愈合，减少疤痕。它的作用是增加伤口周围的血管再生和加快组织重建。
该研究结果将发表在1月26日的Journal of Experimental Medicine上。
Martin教授说，白血细胞（巨噬细胞），运送到伤口细胞的化学信号，以及骨桥蛋白本身都可做为靶标，用于研制改善皮肤伤口愈合或其它纤维化组织修复的药物。我们希望不久以后，这种疗法能够用于临床。
Martin教授实验室和其他人之前的研究，包括人类在内的许多物种的胚胎，愈合伤口不留疤痕。现在看来，在成年人中同样的情况也可能属实。
生物谷推荐原始出处：
Published online 7 January 2008
doi:10.1084/jem.20071412
The Journal of Experimental Medicine, Vol. 205, No. 1, 43-51
Molecular mechanisms linking wound inflammation and fibrosis: knockdown of osteopontin leads to rapid repair and reduced scarring
Ryoichi Mori1,2, Tanya J. Shaw1, and Paul Martin1,2
1 Departments of Physiology and 2 Biochemistry, School of Medical Sciences, University of Bristol, Bristol BS8 1TD, UK
CORRESPONDENCE Paul Martin: paul.martin@bristol.ac.uk
Previous studies of tissue repair have revealed osteopontin (OPN) to be up-regulated in association with the wound inflammatory response. We hypothesize that OPN may contribute to inflammation-associated fibrosis. In a series of in vitro and in vivo studies, we analyze the effects of blocking OPN expression at the wound, and determine which inflammatory cells, and which paracrine factors from these cells, may be responsible for triggering OPN expression in wound fibroblasts. Delivery of OPN antisense oligodeoxynucleotides into mouse skin wounds by release from Pluronic gel decreases OPN protein levels at the wound and results in accelerated healing and reduced granulation tissue formation and scarring. To identify which leukocytic lineages may be responsible for OPN expression, we cultured fibroblasts in macrophage-, neutrophil-, or mast cell–conditioned media (CM), and found that macrophage- and mast cell–secreted factors, specifically platelet-derived growth factor (PDGF), induced fibroblast OPN expression. Correspondingly, Gleevec, which blocks PDGF receptor signaling, and PDGF-Rβ–neutralizing antibodies, inhibited OPN induction by macrophage-CM. These studies indicate that inflammation-triggered expression of OPN both hinders the rate of repair and contributes to wound fibrosis. Thus, OPN and PDGF are potential targets for therapeutic modulation of skin repair to improve healing rate and quality.
