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成纤维细胞引起的胶原凝胶收缩需要细胞纤连蛋白而非血浆纤连蛋白。

Collagen gel contraction by fibroblasts requires cellular fibronectin but not plasma fibronectin.

作者信息

Asaga H, Kikuchi S, Yoshizato K

机构信息

Department of Biology, Faculty of Science, Tokyo Metropolitan University, Japan.

出版信息

Exp Cell Res. 1991 Mar;193(1):167-74. doi: 10.1016/0014-4827(91)90552-6.

Abstract

Fibroblasts embedded in three-dimensional lattices of collagen fibrils have been known to require serum constituents to induce a cell-mediated contraction of collagen gels. The gel contraction was studied with human skin fibroblasts cultured in the presence of fetal bovine serum (FBS). Removal of bovine serum fibronectin (sFN) from FBS did not affect the extent of gel contraction. Gel contraction occurred in serum-free defined media. Therefore, it is concluded that sFN is not required for gel contraction. That cellular FN (cFN) synthesized and secreted by fibroblasts plays a crucial role in gel contraction was suggested by the following experiments: (1) We obtained monoclonal antibodies (mAb A3A5) against fibroblast surface antigens, which suppressed the fibroblast-mediated gel contraction. Immunoblot analyses showed that mAb A3A5 recognizes cFN secreted by human fibroblasts and human plasma FN (pFN), but not bovine sFN in FBS used for culture. (2) Addition of rabbit antisera, which recognize human cFN, to a serum-free gel culture inhibited contraction. Uninvolvement of human pFN in gel contraction was further confirmed by the fact that neither pretreatment of fibroblasts with excess amounts of human pFN nor the presence of excess amounts of human pFN in gels affected the extent of gel contraction. This study seems to be the first demonstration of functional difference between cFN and pFN (or sFN) and proposes a novel mode of binding of fibroblasts with collagen fibrils via cFN during cell-mediated collagen morphogenesis.

摘要

已知包埋在胶原纤维三维晶格中的成纤维细胞需要血清成分来诱导胶原凝胶的细胞介导收缩。在胎牛血清(FBS)存在的情况下,用人皮肤成纤维细胞研究了凝胶收缩。从FBS中去除牛血清纤连蛋白(sFN)并不影响凝胶收缩的程度。在无血清限定培养基中发生了凝胶收缩。因此,得出结论,凝胶收缩不需要sFN。以下实验表明,成纤维细胞合成和分泌的细胞纤连蛋白(cFN)在凝胶收缩中起关键作用:(1)我们获得了针对成纤维细胞表面抗原的单克隆抗体(mAb A3A5),该抗体抑制了成纤维细胞介导的凝胶收缩。免疫印迹分析表明,mAb A3A5识别由人成纤维细胞分泌的cFN和人血浆纤连蛋白(pFN),但不识别用于培养的FBS中的牛sFN。(2)向无血清凝胶培养物中添加识别人类cFN的兔抗血清可抑制收缩。通过用过量人pFN预处理成纤维细胞或凝胶中存在过量人pFN均不影响凝胶收缩程度这一事实,进一步证实了人pFN与凝胶收缩无关。这项研究似乎首次证明了cFN和pFN(或sFN)之间的功能差异,并提出了在细胞介导的胶原形态发生过程中,成纤维细胞通过cFN与胶原纤维结合的新模式。

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