Emodin-mediated cross-linking enhancement for extracellular matrix homeostasis

被引:3
作者
Jian, Lihua [1 ]
Zhang, Chen [1 ]
Chen, Guangfeng [1 ]
Shi, Xiujuan [1 ]
Qiu, Yu [1 ]
Xue, Yunyun [1 ]
Yang, Shuzhang [1 ]
Lu, Lixia [1 ]
Yuan, Qionglan [1 ]
Xu, Guotong [1 ]
Ying, Ming [1 ,2 ]
Liu, Xiaoqing [1 ,2 ]
机构
[1] Tongji Univ, Sch Med, Shanghai Peoples Hosp 10, Shanghai 200092, Peoples R China
[2] Shenzhen Univ, Coll Life Sci, Shenzhen, Peoples R China
基金
中国国家自然科学基金;
关键词
Emodin; Extracellular matrix (ECM); Lysyl oxidase-like 1 (LOXL1); Cross-linking; LYSYL OXIDASE; BIOLOGICAL ROLES; SKIN EQUIVALENT; IN-VITRO; COLLAGEN; PROTEIN; GENE; MICE; FIBULIN-5; FIBERS;
D O I
10.1016/j.bbrc.2014.03.052
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The extracellular matrix (ECM) is an essential element of mammalian organisms, and its cross-linking formation plays a vital role in ECM development and postnatal homeostasis. Defects in cross-link formation caused by aging, genetic, or environmental factors are known to cause numerous diseases in mammals. To augment the cross-linking formation of ECM, the present study established a ZsGreen reporter system controlled by the promoter of lysyl oxidase-like I gene (L0XL1), which serves as both a scaffold element and a cross-linking enzyme in the ECM. By using this system in a drug screen, we identified erhodin as a strong enhancer of LOXL1 expression that promoted cross-linking formation of ECM in all the tested systems, including human fibroblast cells, cultured human skin tissues, and animals that received long-term emodin treatment. Collectively, the results suggest that emodin may serve as an effective drug or supplement for ECM homeostasis. (C) 2014 Elsevier Inc. All rights reserved.
引用
收藏
页码:1022 / 1028
页数:7
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