Functions of the Wnt/β-catenin pathway in an anemia-induced zebrafish model of cardiomyopathy are location dependent.
Functions of the Wnt/β-catenin pathway in an anemia-induced zebrafish model of cardiomyopathy are location dependent.
复制标题
Wnt/β-连环蛋白途径在贫血引起的斑马鱼心肌病模型中的功能是位置依赖性的。
DOI：
10.1016/j.bbrc.2011.10.100
复制
发表时间：
2011
影响因子：
3.1
通讯作者：
Xu,Xiaolei
中科院分区：
文献类型：
--
作者：
Hoage,Tiffany;Sun,Xiaojing;Xu,Xiaolei
Recent evidence that the heart is not a terminally-differentiated organ has provided more credence to investigations of pathways involved in inducing cardiomyocyte (CM) hyperplasia as a therapy for heart disease. Here, we leveraged zebrafish as a novel vertebrate model of cardiomyopathy to explore the therapeutic potential based on the Wnt/β-catenin signaling. In the anemia-induced zebrafish model of cardiomyopathy (tr265), we detected differently regulated CM hyperplasia and CM hypertrophy in the compact region and the trabecular region. To assess the effects of the Wnt/β-catenin pathway on these two regions, the anemia line was crossed with heat shock-inducible transgenic fish to upregulate or downregulate the pathway. Upregulation resulted in increased cardiomyocyte hyperplasia in the heart and increased cardiomyocyte hypertrophy in the trabecular region, while downregulation resulted in reduced cardiomyocyte hyperplasia in the heart and reduced cardiomyocyte hypertrophy in the trabecular region. Importantly, upregulation of the pathway resulted in improved fish survival, while downregulation decreased it. In summary, our data suggested that (1) the compact region and the trabecular region respond differently during cardiac remodeling; (2) activation of the Wnt/β-catenin pathway might exert a cardioprotective function via promoting cardiomyocyte hyperplasia.
