| Summary: | 碩士 === 國立臺灣大學 === 動物學研究所 === 100 === Lysophosphatidic acid, LPA, is a structurally simple lysophospholipid. Derived from phospholipids through autotaxin catalyzation, LPA acts as an extracellular signaling molecule that activates various receptors, LPA1-6. Activation of these receptors induces wound healing, cancer progression, cardiovascular function, nervous system regulation, reproduction, platelet activation, hair growth, etc. To clarify the function of different LPA receptors, several knockout animals have been obtained. While the autotaxin deficient mice expressed the phenotype of embryonic lethality due to vascular defects, none of the single or double deficient LPA1-3 mice expressed similar phenotypes. In this study, I investigate the physiological roles of LPA4, which is structurally distinct from LPA1-3, using zebrafish as a model. LPA4 morpholino was microinjected into one-cell stage zebrafish embryo to knock down the expression level of LPA4 in embryos. In day two, edema around the pericardial region was observed, suggesting a vascular leakage or failure of lymphatic vessels to absorb body fluids in the LPA4 deficient embryos, which was similar to the result of a previous study where LPA1 was found to be essential for lymphatic vessel development in zebrafish. In addition, a significant decrease in heart rate and blood flow was observed in some individuals. Furthermore, the number of intersegmental vessels decreased, suggesting abnormal blood vessel development. However, the dextran uptake was not affected in the LPA4 knock down embryos, suggesting that the development of lymphatic vessels was normal. We conclude that LPA4 may regulate the vascular development in zebrafish.
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