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Hyaluronan in tissue injury and repair.
Annual Review of Cell and Developmental Biology ( IF 11.4 ) Pub Date : 2007-05-18 , DOI: 10.1146/annurev.cellbio.23.090506.123337
Dianhua Jiang 1 , Jiurong Liang , Paul W Noble
Affiliation  

A hallmark of tissue injury and repair is the turnover of extracellular matrix components. This review focuses on the role of the glycosaminoglycan hyaluronan in tissue injury and repair. Both the synthesis and degradation of extracellular matrix are critical contributors to tissue repair and remodeling. Fragmented hyaluronan accumulates during tissue injury and functions in ways distinct from the native polymer. There is accumulating evidence that hyaluronan degradation products can stimulate the expression of inflammatory genes by a variety of immune cells at the injury site. CD44 is the major cell-surface hyaluronan receptor and is required to clear hyaluronan degradation products produced during lung injury; impaired clearance of hyaluronan results in persistent inflammation. However, hyaluronan fragment stimulation of inflammatory gene expression is not dependent on CD44 in inflammatory macrophages. Instead, hyaluronan fragments utilize both Toll-like receptor (TLR) 4 and TLR2 to stimulate inflammatory genes in macrophages. Hyaluronan also is present on the cell surface of lung alveolar epithelial cells and provides protection against tissue damage by interacting with TLR2 and TLR4 on these parenchymal cells. The simple repeating structure of hyaluronan appears to be involved in a number of important aspects of noninfectious tissue injury and repair that are dependent on the size and location of the polymer as well as the interacting cells. Thus, the interactions between the endogenous matrix component hyaluronan and its signaling receptors initiate inflammatory responses, maintain structural cell integrity, and promote recovery from tissue injury.

中文翻译:

乙酰透明质酸在组织损伤和修复中。

组织损伤和修复的标志是细胞外基质成分的更新。这篇综述集中在糖胺聚糖透明质酸在组织损伤和修复中的作用。细胞外基质的合成和降解都是组织修复和重塑的关键因素。碎片透明质酸在组织损伤期间积累,并以与天然聚合物不同的方式发挥作用。越来越多的证据表明,透明质酸降解产物可以通过损伤部位的多种免疫细胞刺激炎症基因的表达。CD44是主要的细胞表面透明质酸受体,是清除肺损伤期间产生的透明质酸降解产物所必需的;透明质酸清除能力受损会导致持续性炎症。然而,乙酰透明质酸片段对炎性基因表达的刺激不依赖于炎性巨噬细胞中的CD44。相反,透明质酸片段利用Toll样受体(TLR)4和TLR2刺激巨噬细胞中的炎症基因。透明质酸也存在于肺泡上皮细胞的细胞表面,并通过与这些实质细胞上的TLR2和TLR4相互作用而提供针对组织损伤的保护。透明质酸的简单重复结构似乎涉及非感染性组织损伤和修复的许多重要方面,这些方面取决于聚合物以及相互作用细胞的大小和位置。因此,内源性基质成分透明质酸与其信号受体之间的相互作用会引发炎症反应,维持细胞结构的完整性,
更新日期:2019-11-01
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