Regulation of fibroblast-mediated collagen gel contraction by platelet-derived growth factor, interleukin-1 alpha and transforming growth factor-beta 1.
Regulation of fibroblast-mediated collagen gel contraction by platelet-derived growth factor, interleukin-1 alpha and transforming growth factor-beta 1.
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发表时间：
1992-06
影响因子：
4
通讯作者：
A. Tingström;C. Heldin;K. Rubin
中科院分区：
文献类型：
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作者：
A. Tingström;C. Heldin;K. Rubin
我们研究了三种巨噬细胞衍生的细胞因子，血小板衍生生长因子（PDGF），转化生长因子-β 1（TGF-β 1）和白细胞介素-1 α（IL-1 α）对人包皮成纤维细胞填充的I型胶原蛋白凝胶收缩的影响。收缩被量化为凝胶重量的损失。发现PDGF-AA和PDGF-BB均诱导快速胶原-凝胶收缩。TGF-β 1也刺激凝胶收缩，但与PDGF刺激的收缩相比，延迟发作且速率较慢。分别识别PDGF-AA和PDGF-BB的兔多克隆IgG特异性抑制相应PDGF同种型的作用。然而，TGF-β 1的刺激作用不受任何抗PDGF抗体的影响。PDGF刺激收缩的能力变得不太明显，在胶原凝胶培养生长在生长因子的情况下，在几天的时间。在相同条件下，TGF-β 1的刺激作用没有降低。对PDGF的反应降低可能是由于胶原凝胶中生长的成纤维细胞上的张力降低，因为与附着的胶原凝胶上的成纤维细胞相比，自由浮动凝胶上的成纤维细胞显示出PDGF-BB诱导的PDGF β受体聚集体的显著减少。IL-1 α抑制初始胶原凝胶收缩，并在后期诱导胶原凝胶的可见降解，推测是由于胶原酶活性的产生。IL-1 α和PDGF-BB的组合刺激初始胶原凝胶收缩，尽管不如单独的PDGF-BB有效。（250字处删节）
We have examined the effects of three macrophage-derived cytokines, platelet-derived growth factor (PDGF), transforming growth factor-beta 1 (TGF-beta 1) and interleukin-1 alpha (IL-1 alpha) on the contraction of collagen type I gels populated by human foreskin fibroblasts. Contraction was quantified as loss in gel weight. Both PDGF-AA and PDGF-BB were found to induce a rapid collagen-gel contraction. TGF-beta 1 also stimulated gel contraction but with a delayed onset and at a slower rate than the PDGF-stimulated contraction. Rabbit polyclonal IgGs recognizing PDGF-AA and PDGF-BB, respectively, specifically inhibited the effects of the corresponding PDGF isoforms. However, the stimulatory effect of TGF-beta 1 was not affected by any of the anti-PDGF antibodies. The ability of PDGF to stimulate contraction became less pronounced in collagen gel cultures grown in the absence of growth factors over periods of several days. Under the same conditions, the stimulatory effect of TGF-beta 1 was not reduced. The reduced response to PDGF may be due to reduced tension on fibroblasts growing in collagen gels, since fibroblasts on free-floating gels showed a marked reduction in PDGF-BB-induced PDGF beta-receptor aggregates when compared to fibroblasts on attached collagen gels. IL-1 alpha inhibited initial collagen gel contraction, and at later stages induced a visible degradation of the collagen gels, presumably due to the generation of collagenase activity. The combination of IL-1 alpha and PDGF-BB stimulated initial collagen gel contraction, although less effectively than PDGF-BB alone.(ABSTRACT TRUNCATED AT 250 WORDS)