Glucocorticoid-regulated gene expression during cutaneous wound repair.
Glucocorticoid-regulated gene expression during cutaneous wound repair.
复制标题
DOI：
10.1016/s0083-6729(00)59008-6
复制
发表时间：
2000-01-01
影响因子：
--
通讯作者：
Werner, S
中科院分区：
文献类型：
--
作者：
Beer, H D;Fassler, R;Werner, S
糖皮质激素对伤口愈合过程产生有害影响，这被认为是由于这些类固醇的抗炎作用。此外，最近的研究表明，糖皮质激素调节伤口部位各种基因的表达，这些基因可能编码伤口修复过程中的关键角色。采用小鼠全层切除创面愈合模型，分析地塞米松对正常和损伤皮肤中各种细胞因子、生长因子、酶和细胞外基质分子表达的影响。我们证明，促炎细胞因子白介素-1 α和- β、肿瘤坏死因子α、角化细胞生长因子、转化生长因子β 1、β 2和β 3及其受体、血小板源性生长因子及其受体、腱素- c、基质溶解素-2、巨噬细胞金属弹性酶和参与生成一氧化氮的酶是糖皮质激素在损伤皮肤中作用的靶标。这些结果表明，抗炎类固醇至少在一定程度上通过影响这些关键调节分子的表达来抑制伤口修复。
Glucocorticoids exert a deleterious effect on the wound healing process, which has been suggested to result from the anti-inflammatory action of these steroids. In addition, recent studies have demonstrated that glucocorticoids regulate the expression of various genes at the wound site which are likely to encode key players in the wound repair process. Using a murine full-thickness excisional wound healing model, we analyzed the effect of dexamethasone on the expression of various cytokines, growth factors, enzymes, and extracellular matrix molecules in normal and wounded skin. We demonstrate that the proinflammatory cytokines interleukin-1 alpha and -beta, tumor necrosis factor alpha, keratinocyte growth factor, transforming growth factors beta 1, beta 2, and beta 3 and their receptors, platelet-derived growth factors and their receptors, tenascin-C, stromelysin-2, macrophage metalloelastase, and enzymes involved in the generation of nitric oxide are targets of glucocorticoid action in wounded skin. These results indicate that anti-inflammatory steroids inhibit wound repair at least in part by influencing the expression of these key regulatory molecules.