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首页> 外文期刊>American Journal of Physiology >Collagen I matrix turnover is regulated by fibronectin polymerization
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Collagen I matrix turnover is regulated by fibronectin polymerization

机译：胶原I基质的转换受纤连蛋白聚合作用的调节

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Extracellular matrix (ECM) remodeling occurs during normal homeostasis and also plays an important role during development, tissue repair, and in various disease processes. ECM remodeling involves changes in the synthesis, deposition, and degradation of ECM molecules. ECM molecules can be degraded extracellularly, as well as intracellularly following endocytosis. Our data show that the ECM protein fibronectin is an important regulator of ECM remodeling. We previously showed that agents that inhibit the polymerization of fibronectin into ECM fibrils promote the loss of preexisting fibronectin matrix and accelerate fibronectin endocytosis and degradation. In this paper we show that inhibition of fibronectin polymerization leads to the loss of collagen I matrix fibrils and a corresponding increase in the levels of endocytosed collagen I. In contrast, manipulations that stabilize fibronectin matrix fibrils, such as caveolin-1 depletion, stabilize collagen I matrix fibrils and cause a decrease in ECM collagen I endocytosis. Our data also show that endocytosis of ECM collagen I is regulated by both β1 integrins and Endo180/urokinase plasminogen activator associated protein (uPARAP). Unexpectedly, Endo180/uPARAP was also shown to promote the endocytosis of fibronectin from the ECM. These data demonstrate that fibronectin polymerization regulates the remodeling of ECM collagen I, in part, by regulating collagen I endocytosis. Furthermore, these data show that processes that regulate ECM deposition coordinately regulate the removal of proteins from the ECM. These data highlight the complexity of ECM remodeling. This multifaceted regulatory process may be important to ensure tight regulation of ECM fibronectin and collagen I levels.
机译：细胞外基质（ECM）重塑发生在正常的体内平衡过程中，并且在发育，组织修复以及各种疾病过程中也起着重要作用。 ECM重塑涉及ECM分子合成，沉积和降解的变化。内吞后，ECM分子可在细胞外以及细胞内降解。我们的数据表明，ECM蛋白纤连蛋白是ECM重塑的重要调节剂。先前我们发现抑制纤连蛋白聚合成ECM纤丝的试剂会促进原有纤连蛋白基质的丢失，并加速纤连蛋白的内吞作用和降解。在本文中，我们表明抑制纤连蛋白聚合导致胶原蛋白I基质原纤维的损失和相应增加的内吞胶原蛋白I的水平。相反，稳定纤连蛋白基质原纤维的操作（例如小窝蛋白-1耗竭）可稳定胶原蛋白。 I基质原纤维并导致ECM胶原I内吞作用减少。我们的数据还表明，ECM胶原蛋白I的内吞作用受β1整合素和Endo180 /尿激酶纤溶酶原激活物相关蛋白（uPARAP）的调节。出乎意料的是，还显示Endo180 / uPARAP可以促进ECM中纤连蛋白的内吞作用。这些数据表明纤连蛋白聚合部分地通过调节胶原蛋白I的内吞作用来调节ECM胶原蛋白I的重塑。此外，这些数据表明，调节ECM沉积的过程可协调地调节蛋白质从ECM中的去除。这些数据突出了ECM重塑的复杂性。这一多方面的调节过程对于确保ECM纤连蛋白和胶原蛋白I水平的严格调节可能很重要。

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