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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >Regulation of corneal inflammation by neutrophil-dependent cleavage of keratan sulfate proteoglycans as a model for breakdown of the chemokine gradient.
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Regulation of corneal inflammation by neutrophil-dependent cleavage of keratan sulfate proteoglycans as a model for breakdown of the chemokine gradient.

机译：通过中性粒细胞依赖性硫酸角质素蛋白聚糖的裂解来调节角膜炎症，作为趋化因子梯度分解的模型。

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摘要

Keratocan and lumican are small, leucine-rich repeat KSPGs in the extracellular matrix (ECM) of the mammalian cornea, whose primary role is to maintain corneal transparency. In the current study, we examined the role of these proteoglycans in the breakdown of the chemokine gradient and resolution of corneal inflammation. LPS was injected into the corneal stroma of C57BL/6 mice, and corneal extracts were examined by immunoblot analysis. We found reduced expression of the 52-kD keratocan protein after 6 h and conversely, increased expression of 34/37 kD immunoreactive products. Further, appearance of the 34/37-kD proteins was dependent on neutrophil infiltration to the cornea, as the appearance of these products was coincident with neutrophil infiltration, and the 34/37-kD products were not detected in explanted corneas or in CXCR2(-/-) corneas with deficient neutrophil recruitment. Furthermore, the 34/37-kD products and CXCL1/KC were detected in the anterior chamber, into which the corneal stroma drains; and CXCL1/KC was elevated significantly in keratocan(-/-) and lumican(-/-) mice. Together, these findings indicate that the inflammatory response in the cornea is regulated by proteoglycan/CXCL1 complexes, and their diffusion into the anterior chamber is consistent with release of a chemokine gradient and resolution of inflammation.
机译：角蛋白聚糖和lumican是哺乳动物角膜细胞外基质（ECM）中富含亮氨酸的小重复KSPG，其主要作用是维持角膜透明性。在当前的研究中，我们检查了这些蛋白聚糖在趋化因子梯度分解和角膜炎症消退中的作用。将LPS注射到C57BL / 6小鼠的角膜基质中，并通过免疫印迹分析检查角膜提取物。我们发现6小时后52 kD角蛋白聚糖蛋白的表达减少，反之，34/37 kD免疫反应产物的表达增加。此外，34 / 37-kD蛋白的出现取决于嗜中性粒细胞向角膜的浸润，因为这些产物的出现与嗜中性白细胞的浸润一致，并且在移出的角膜或CXCR2中未检测到34 / 37-kD产物（ -/-）中性粒细胞募集不足的角膜。此外，在前房中检出了34 / 37-kD产物和CXCL1 / KC，角膜基质向其中排出。和CXCL1 / KC在keratocan（-/-）和lumican（-/-）小鼠中显着升高。在一起，这些发现表明角蛋白中的炎症反应是由蛋白聚糖/ CXCL1复合物调节的，它们扩散到前房与趋化因子梯度的释放和炎症的消退是一致的。

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