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Harmful algal blooms: mechanisms, monitoring, and prevention in a rapidly changing world
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Okadaic acid exposure inhibits the development of neural crest cells through the EMT proces
P-B1-17-S
Yu-hu Jiao* , Key Laboratory of Aquatic Eutrophication and Control of Harmful Algal Blooms of Guangdong Higher Education Institute, College of Life Science and Technology, Jinan University, Guangzhou 510632, China
Guang Wang, Division of Histology and Embryology, Key Laboratory for Regenerative Medicine of the Ministry of Education, Medical College, Jinan University, Guangzhou 510632, China
Hong-ye Li, Key Laboratory of Aquatic Eutrophication and Control of Harmful Algal Blooms of Guangdong Higher Education Institute, College of Life Science and Technology, Jinan University, Guangzhou 510632, China
Jie-sheng Liu, Key Laboratory of Aquatic Eutrophication and Control of Harmful Algal Blooms of Guangdong Higher Education Institute, College of Life Science and Technology, Jinan University, Guangzhou 510632, China
Xuesong Yang, Division of Histology and Embryology, Key Laboratory for Regenerative Medicine of the Ministry of Education, Medical College, Jinan University, Guangzhou 510632, China
Wei-dong Yang, Key Laboratory of Aquatic Eutrophication and Control of Harmful Algal Blooms of Guangdong Higher Education Institute, College of Life Science and Technology, Jinan University, Guangzhou 510632, China
Presenter Email: 739933791@qq.com |
| Okadaic acid (OA), the main component of diarrheic shellfish poisoning (DSP), is a potent phosphatase specific inhibitor and neurotoxin. However, it is still unclear how OA exposure could affect neural crest cells (NCCs) generation in early embryo development. In this study, using a chick embryo model, we investigated effects of OA exposure on neural crest cells during embryonic development. We found that OA exposure could lead to craniofacial bone defects in the developing chick embryo, and delay the development of gastrulating chick embryos. Immunofluorescence staining of HNK-1, PAX7, and Ap-2¦Á indicated that cranial NCCs generation was inhibited after OA exposure. Double immunofluorescent staining (Ap-2¦Á and PHIS3 or PAX7 and c-Caspase3) suggested that OA exposure inhibited both NCCs proliferation and apoptosis. Furthermore, Msx1 and BMP4 expression were down-regulated in the developing neural tube. It revealed that production of NCCs was inhibited. We also determined that expression of EMT-related adhesion molecules, Cad6B and E-Cadherin, for example, and found that they were altered. In all, OA exposure could affect the development of neural crest cells, which in turn causes defective cranial bone development.
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