Functions of hypoxia signaling on apelin expression during zebrafish development

• Main Authors: Chou,Chen-Tian, 周成恬
• Other Authors: Hu,Chin-Hwa
• Format: Others
• Language: zh-TW
• Published: 2014
• Online Access: http://ndltd.ncl.edu.tw/handle/77564y

碩士 === 國立臺灣海洋大學 === 生物科技研究所 === 102 === Abstract Apelin (Apln) is an adipokine that has been identified as an endogenous ligand for the APJ receptor. Human Apelin gene is located in the long arm of the X chromosome and encodes a 77 amino acid prepropreptide that could be further cleaved into several short peptides. Apelin has a wide range of physiological functions, including NO-dependent vasodilation, cardiac contractility, and endothelial cell proliferation. The apelin/APJ (apelin receptor) system acts as critical mediator of cardiovascular homeostasis and is involved in the pathophysiology of cardiovascular diseases. It also acts as an activator of angiogenesis. Apln expression is induced by hypoxia in cultured endothelial and vascular smooth muscle cells due to HIF1 binding to the enhancer sequence. Apelin is also expressed during developmental stage. Here I have investigated the function of HIFα in apln transcription in zebrafish embryos. It appears that the HIF-signaling pathways involve in apln regulation. Depletion of hif1α or hif2α abrogated apln transcription in embryos. By contrast, hypoxia induces apln transcription, suggesting that the basal apln transcription in zebrafish embryos is controlled by both HIF1α and HIF2α. Keywords: zebrafish, Apelin, HIF1α, HIF2α, hypoxia