Signal transduction pathways activated during fibroblast contraction of collagen matrices.
Signal transduction pathways activated during fibroblast contraction of collagen matrices.
复制标题
胶原基质的成纤维细胞收缩期间激活信号转导途径。
DOI：
10.1007/978-3-642-58456-5_7
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发表时间：
1999
期刊：
影响因子：
--
通讯作者：
Grinnell,F
中科院分区：
文献类型：
--
作者：
Grinnell,F
在胶原基质中培养的成纤维细胞已被用于建立伤口收缩过程的体外模型。漂浮基质的收缩类似于创面初期的收缩，附着基质的收缩类似于肉芽组织的形成，应力基质的收缩类似于修复结束时的肉芽组织收缩和退缩。我们实验室的研究主要集中在应力矩阵的收缩上。应激性基质收缩的基本成分导致细胞质膜外翻，肌动蛋白细胞骨架破坏，钙离子摄取，环磷酸腺苷(CAMP)和丝裂原激活蛋白(MAP)信号通路的刺激，以及c-fos和其他即刻早期基因的转录激活。应激基质收缩的刺激成分(由血清或溶血磷脂酸刺激)导致肌动蛋白细胞骨架收缩和生长因子脱敏。随后，细胞变得静止，并通过细胞凋亡而退化。
Fibroblasts cultured in collagen matrices have been used to develop in vitro models of the wound contraction process. Contraction of floating matrices resembles initial wound contraction, contraction of attached matrices resembles granulation tissue formation, and contraction of stressed matrices resembles granulation tissue contraction and regression at the end of repair. Studies in our laboratory have focused on contraction of stressed matrices. The basal component of stressed matrix contraction results in plasma-membrane ectocytosis, actin cytoskeletal disruption, Ca2+ uptake, stimulation of cyclic adenosine monophosphate (cAMP) and mitogen-activated protein (MAP) kinase signaling pathways, and transcriptional activation of c-fos and other immediate early genes. The stimulated component of stressed matrix contraction (stimulated by serum or lysophosphatidic acid) results in actin cytoskeletal retraction and growth-factor desensitization. Subsequently, the cells become quiescent and regress through apoptosis.