Pierce G F, Vande Berg J, Rudolph R, Tarpley J, Mustoe T A
Department of Experimental Pathology, Amgen Inc., Thousand Oaks, California 91320.
Am J Pathol. 1991 Mar;138(3):629-46.
Recombinant platelet-derived growth factor (PDGF) and transforming growth factor beta 1 (TGF-beta 1) influence the rate of extracellular matrix formed in treated incisional wounds. Because incisional healing processes are difficult to quantify, a full-thickness excisional wound model in the rabbit ear was developed to permit detailed analyses of growth-factor-mediated tissue repair. In the present studies, quantitative and qualitative differences in acute inflammatory cell influx, glycosaminoglycan (GAG) deposition, collagen formation, and myofibroblast generation in PDGF-BB (BB homodimer)- and TGF-beta 1-treated wounds were detected when analyzed histochemically and ultrastructurally. Although both growth factors significantly augmented extracellular matrix formation and healing in 10-day wounds compared with controls (P less than 0.002). PDGF-BB markedly increased macrophage influx and GAG deposition, whereas TGF-beta 1 selectively induced significantly more mature collagen bundles at the leading edge of new granulation tissue (P = 0.007). Transforming growth factor-beta 1-treated wound fibroblasts demonstrated active collagen fibrillogenesis and accretion of subfibrils at the ultrastructural level. Myofibroblasts, phenotypically modified fibroblasts considered responsible for wound contraction, were observed in control, but were absent in early growth-factor-treated granulating wounds. These results provide important insights into the mechanisms of soft tissue repair and indicate that 1) PDGF-BB induces an inflammatory response and provisional matrix synthesis within wounds that is qualitatively similar but quantitatively increased compared with normal wounds; 2) TGF-beta 1 preferentially triggers synthesis and more rapid maturation of collagen within early wounds; and 3) both growth factors inhibit the differentiation of fibroblasts into myofibroblasts, perhaps because wound contraction is not required, due to increased extracellular matrix synthesis.
重组血小板衍生生长因子(PDGF)和转化生长因子β1(TGF-β1)会影响处理过的切口伤口中细胞外基质的形成速率。由于切口愈合过程难以量化,因此建立了兔耳全层切除伤口模型,以便对生长因子介导的组织修复进行详细分析。在本研究中,当对PDGF-BB(BB同型二聚体)和TGF-β1处理的伤口进行组织化学和超微结构分析时,检测到急性炎症细胞流入、糖胺聚糖(GAG)沉积、胶原蛋白形成和成肌纤维细胞生成方面的定量和定性差异。尽管与对照组相比,两种生长因子均显著增强了10天伤口中的细胞外基质形成和愈合(P<0.002)。PDGF-BB显著增加巨噬细胞流入和GAG沉积,而TGF-β1选择性地在新肉芽组织前沿诱导显著更多成熟的胶原束(P = 0.007)。TGF-β1处理的伤口成纤维细胞在超微结构水平上表现出活跃的胶原纤维形成和亚纤维的积聚。成肌纤维细胞是一种表型改变的成纤维细胞,被认为与伤口收缩有关,在对照组中可见,但在早期生长因子处理的肉芽伤口中不存在。这些结果为软组织修复机制提供了重要见解,并表明:1)PDGF-BB在伤口内诱导炎症反应和临时基质合成,与正常伤口相比,其性质相似但数量增加;2)TGF-β1优先触发早期伤口内胶原蛋白的合成和更快成熟;3)两种生长因子均抑制成纤维细胞向肌成纤维细胞的分化,这可能是由于细胞外基质合成增加,不需要伤口收缩。