Alteration of the chemotactic response of human skin fibroblasts to PDGF by growth factors.
Alteration of the chemotactic response of human skin fibroblasts to PDGF by growth factors.
复制标题
生长因子改变人皮肤成纤维细胞对 PDGF 的趋化反应。
DOI：
10.1006/excr.1994.1143
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发表时间：
1994
影响因子：
3.7
通讯作者：
Y. Ishibashi
中科院分区：
文献类型：
--
作者：
Y. Soma;K. Takehara;Y. Ishibashi
血小板衍生生长因子(PDGF)是一种强有力的成纤维细胞有丝分裂原和趋化物质。在伤口愈合的早期阶段。PDGF是从聚集的血小板中释放出来的，人们认为它的趋化活性可能在结缔组织细胞涌入伤口部位起关键作用。利用Boyden小室实验，我们研究了改变人皮肤成纤维细胞对PDGF迁移反应的因素。这种反应与细胞的生长状态有关，即在低细胞密度下生长的细胞比密度受阻的静止细胞对PDGF表现出更大的迁移反应。与静止细胞相比，生长细胞的随机迁移水平也较高。血清作用3h后，趋化反应明显降低(>；50%)。细胞与转化生长因子-β(转化生长因子-β)或表皮生长因子预先孵育3小时后，迁移反应减少到非刺激对照的大约一半。相反，经转化生长因子-β或碱性成纤维细胞生长因子处理24小时的细胞对PDGF的趋化反应是对照细胞的两到三倍。转化生长因子-β对PDGF诱导的成纤维细胞迁移的刺激作用表明，转化生长因子-β与PDGF在结缔组织细胞进入人体创面的过程中具有协同作用，这可能解释了转化生长因子-β在体内具有强大的创面愈合活性。
Platelet-derived growth factor (PDGF) is a potent mitogen and chemoattractant for fibroblastic cells. In the early stage of wound healing. PDGF is released from aggregated platelets and it is believed that its chemotactic activity may play a key role in the influx of connective tissue cells into wound sites. Using the Boyden chamber assay, we investigated factors that alter the migratory response of human skin fibroblasts to PDGF. The response was related to the growth state of cells; that is, growing cells at low cell density exhibited a greater migratory response to PDGF than density-arrested quiescent cells. The level of random migration was also elevated in growing cells, compared to quiescent cells. The chemotactic response after 3-h exposure to serum was markedly decreased (> 50%). Three-hour preincubation of the cells with transforming growth factor-beta (TGF-beta) or with epidermal growth factor reduced the migratory response to approximately half that in the nonstimulated control. In contrast, cells treated with TGF-beta or basic fibroblast growth factor for 24 h exhibited a two- to threefold greater chemotactic response to PDGF than control cells. This stimulatory effect of TGF-beta on the fibroblast migration induced by PDGF suggests that TGF-beta acts synergistically with PDGF on the influx of connective tissue cells into human wound sites and may explain the potent wound healing activity of TGF-beta in vivo.