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受损细胞释放的蛋白酶启动伤口愈合。

Initiation of wound healing by proteinases released from damaged cells.

作者信息

Hatanaka M, Tsuboi K

机构信息

Institute for Virus Research, Kyoto University, Japan.

出版信息

Int J Tissue React. 1991;13(5):249-55.

PMID:1806547
Abstract

The wound-healing process is initiated as soon as the tissue is injured. Herein, we demonstrate that c-fos and c-myc mRNA transcripts are promptly increased in the wounded tissue in vivo and in vitro. A buffer solution from scraped serum-starved quiescent fibroblasts, when added to resting fibroblasts, caused an increase of c-fos and c-myc mRNA among the indicator cells. Soluble factors contained in the wounding supernatant are responsible for these phenomena, and we call them wounding factors. Addition of proteinase inhibitors to the culture medium drastically reduced the c-fos mRNA induction by the wounding factors. Exogenously added trypsin or thrombin mimicked the activity of wounding factors. These results suggest that wounding causes soluble factors including various proteinases to be released from the damaged cells, which trigger the adjacent cells to respond to the injury.

摘要

一旦组织受到损伤,伤口愈合过程便立即启动。在此,我们证明,在体内和体外,受伤组织中的c-fos和c-myc信使核糖核酸转录物会迅速增加。从血清饥饿的静止成纤维细胞刮取的缓冲液,当添加到静止的成纤维细胞中时,会导致指示细胞中c-fos和c-myc信使核糖核酸增加。伤口上清液中所含的可溶性因子是造成这些现象的原因,我们将其称为伤口因子。向培养基中添加蛋白酶抑制剂可大幅降低伤口因子对c-fos信使核糖核酸的诱导作用。外源添加的胰蛋白酶或凝血酶模拟了伤口因子的活性。这些结果表明,伤口会导致包括各种蛋白酶在内的可溶性因子从受损细胞中释放出来,从而触发相邻细胞对损伤做出反应。

相似文献

1
Initiation of wound healing by proteinases released from damaged cells.受损细胞释放的蛋白酶启动伤口愈合。
Int J Tissue React. 1991;13(5):249-55.
2
Soluble factors including proteinases released from damaged cells may trigger the wound healing process.包括受损细胞释放的蛋白酶在内的可溶性因子可能会触发伤口愈合过程。
Biochem Biophys Res Commun. 1990 May 16;168(3):1163-70. doi: 10.1016/0006-291x(90)91151-h.
3
[mRNA and protein expression of three growth-related factors and their possible signal transduction pathways in wound healing].[三种生长相关因子在伤口愈合中的mRNA和蛋白质表达及其可能的信号转导途径]
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Antisense targeting of c-fos transcripts inhibits serum- and TGF-beta 1-stimulated PAI-1 gene expression and directed motility in renal epithelial cells.针对c-fos转录本的反义作用抑制血清和转化生长因子-β1刺激的肾上皮细胞中纤溶酶原激活物抑制因子-1基因表达及定向运动。
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Cytoskeleton regulates expression of genes for transforming growth factor-beta 1 and extracellular matrix proteins in dermal fibroblasts.细胞骨架调节真皮成纤维细胞中转化生长因子-β1和细胞外基质蛋白的基因表达。
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Wound healing following injury to vascular smooth muscle cell cultures is modulated by culture under hypergravity.血管平滑肌细胞培养物损伤后的伤口愈合受到超重力培养的调节。
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Effect of Na + flux inhibitors on induction of c-fos, c-myc, and ODC genes during cell cycle.钠离子通量抑制剂对细胞周期中c-fos、c-myc和鸟氨酸脱羧酶基因诱导的影响。
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c-Myc creates an activation loop by transcriptionally repressing its own functional inhibitor, hMad4, in young fibroblasts, a loop lost in replicatively senescent fibroblasts.在年轻的成纤维细胞中,c-Myc通过转录抑制其自身的功能抑制剂hMad4来形成一个激活环,而在复制性衰老的成纤维细胞中这个环会消失。
J Cell Biochem. 2005 Dec 1;96(5):1071-85. doi: 10.1002/jcb.20503.

引用本文的文献

1
Protease cleavage of iron-transferrin augments pyocyanin-mediated endothelial cell injury via promotion of hydroxyl radical formation.铁转铁蛋白的蛋白酶裂解通过促进羟基自由基形成增强绿脓杆菌介导的内皮细胞损伤。
Infect Immun. 1996 Jan;64(1):182-8. doi: 10.1128/iai.64.1.182-188.1996.
2
Protease-cleaved iron-transferrin augments oxidant-mediated endothelial cell injury via hydroxyl radical formation.蛋白酶切割的铁转铁蛋白通过羟基自由基的形成增强氧化剂介导的内皮细胞损伤。
J Clin Invest. 1995 Jun;95(6):2491-500. doi: 10.1172/JCI117950.