Extracellular matrix regulation of inflammation in the healthy and injured spinal cord.
Extracellular matrix regulation of inflammation in the healthy and injured spinal cord.
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DOI：
10.1016/j.expneurol.2013.11.020
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发表时间：
2014-08
影响因子：
5.3
通讯作者：
Popovich, Phillip G.
中科院分区：
文献类型：
--
作者：
Gaudet, Andrew D.;Popovich, Phillip G.
在整个身体中，细胞外基质（ECM）为组织提供结构和组织，并帮助调节细胞迁移和细胞间通讯。在损伤的脊髓（或脑）中，ECM成分和结构的改变无疑会导致再生失败。不太清楚的是，原生和损伤的ECM如何影响椎管内炎症，反过来，神经炎症如何影响CNS损伤后ECM的合成和沉积。在所有组织中，炎症可由ECM破坏引发和传播。损伤或炎症新释放的ECM分子包括透明质酸片段、腱蛋白和硫酸化蛋白聚糖。它们充当“损伤相关分子模式”或“警报器”，即触发并随后放大炎症的内源性蛋白质。激活的炎症细胞反过来通过释放降解酶（包括基质金属蛋白酶（MMPs））进一步损害ECM。脊髓损伤（SCI）后，ECM结构和化学成分的不稳定或改变会影响所有细胞（神经细胞和非神经细胞）的迁移、通讯和存活，而这些细胞对脊髓修复至关重要。通过稳定ECM结构或改变其触发炎症降解效应的能力，有可能创造一个更有利于脊髓损伤后组织修复和轴突可塑性的环境。
Throughout the body, the extracellular matrix (ECM) provides structure and organization to tissues and also helps regulate cell migration and intercellular communication. In the injured spinal cord (or brain), changes in the composition and structure of the ECM undoubtedly contribute to regeneration failure. Less appreciated is how the native and injured ECM influences intraspinal inflammation and, conversely, how neuroinflammation affects the synthesis and deposition of ECM after CNS injury. In all tissues, inflammation can be initiated and propagated by ECM disruption. Molecules of ECM newly liberated by injury or inflammation include hyaluronan fragments, tenascins, and sulfated proteoglycans. These act as “damage-associated molecular patterns” or “alarmins”, i.e., endogenous proteins that trigger and subsequently amplify inflammation. Activated inflammatory cells, in turn, further damage the ECM by releasing degradative enzymes including matrix metalloproteinases (MMPs). After spinal cord injury (SCI), destabilization or alteration of the structural and chemical composition of the ECM affects migration, communication, and survival of all cells – neural and non-neural – that are critical for spinal cord repair. By stabilizing ECM structure or modifying their ability to trigger the degradative effects of inflammation, it may be possible to create an environment that is more conducive to tissue repair and axon plasticity after SCI.
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影响因子：
15.3
作者：
Brambilla, R;Bracchi-Ricard, V;Hu, WH;Frydel, B;Bramwell, A;Karmally, S;Green, EJ;Bethea, JR
通讯作者：
Bethea, JR
影响因子：
5.3
作者：
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通讯作者：
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影响因子：
3.5
作者：
Becker, CG;Schweitzer, J;Becker, T
通讯作者：
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影响因子：
3.4
作者：
Davies, JE;Tang, XF;Davies, SJA
通讯作者：
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影响因子：
3.4
作者：
Ding, QX;Wu, Z;Liu, SJ
通讯作者：
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