Proteoglycan from salmon nasal cartridge promotes in vitro wound healing of fibroblast monolayers via the CD44 receptor

Proteoglycan from salmon nasal cartridge promotes in vitro wound healing of fibroblast monolayers via the CD44 receptor
复制标题

DOI:
10.1016/j.bbrc.2014.12.037
复制
发表时间:
2015-01-16
影响因子:
3.1
通讯作者:
Sokabe, Masahiro
Sokabe, Masahiro
中科院分区:
生物学4区
文献类型:
--
作者:
Ito, Gen;Kobayashi, Takeshi;Sokabe, Masahiro

文献摘要

被引文献

相似文献

蛋白聚糖(PG)参与各种细胞功能,包括细胞生长,粘附和分化;然而,它们的生理作用尚未完全了解。在这项研究中,我们研究了从鲑鱼鼻软骨(SNC-PG)纯化的PG对伤口愈合的影响,使用组织培养的细胞单层,在体外伤口愈合试验。结果表明,SNC-PG通过刺激细胞增殖和细胞迁移,显著促进NIH/3 T3细胞单层伤口闭合。SNC-PG在0.1至10 μ g/ml的浓度下是有效的,但在更高的浓度(100-1000 μ g/ml)下显示出小得多的效果。软骨素酶ABC可消除SNC-PG的作用,表明硫酸软骨素(CS)是SNC-PG中糖胺聚糖(GAG)的主要成分,对SNC-PG的作用至关重要。此外,6-硫酸软骨素(C-6-S),SNC-PG糖胺聚糖的主要CS,可以部分重现SNC-PG的作用,并部分抑制SNC-PG与细胞的结合,表明SNC-PG发挥其作用,通过之间的相互作用SNC-PG中的糖胺聚糖和细胞表面。通过抗CD 44抗体或CD 44敲低的中和作用消除了SNC-PG与细胞的结合以及SNC-PG对伤口闭合的作用。这些结果表明,细胞表面上SNC-PG的富含CS的GAG链和CD 44之间的相互作用是SNC-PG对伤口闭合的作用的原因。(C)2014 Elsevier Inc. All rights reserved.
Proteoglycans (PGs) are involved in various cellular functions including cell growth, adhesion, and differentiation; however, their physiological roles are not fully understood. In this study, we examined the effect of PG purified from salmon nasal cartilage (SNC-PG) on wound closure using tissue-cultured cell monolayers, an in vitro wound-healing assay. The results indicated that SNC-PG significantly promoted wound closure in NIH/3T3 cell monolayers by stimulating both cell proliferation and cell migration. SNC-PG was effective in concentrations from 0.1 to 10 mu g/ml, but showed much less effect at higher concentrations (100-1000 mu g/ml). The effect of SNC-PG was abolished by chondroitinase ABC, indicating that chondroitin sulfates (CSs), a major component of glycosaminoglycans (GAGs) in SNC-PG, are crucial for the SNC-PG effect. Furthermore, chondroitin 6-sulfate (C-6-S), a major CS of SNC-PG GAGs, could partially reproduce the SNC-PG effect and partially inhibit the binding of SNC-PG to cells, suggesting that SNC-PG exerts its effect through an interaction between the GAGs in SNC-PG and the cell surface. Neutralization by anti-CD44 antibodies or CD44 knockdown abolished SNC-PG binding to the cells and the SNC-PG effect on wound closure. These results suggest that interactions between CS-rich GAG-chains of SNC-PG and CD44 on the cell surface are responsible for the SNC-PG effect on wound closure. (C) 2014 Elsevier Inc. All rights reserved.