|ZFIN ID: ZDB-PUB-181026-24|
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Pparα deficiency inhibits the proliferation of neuronal and glial precursors in the zebrafish central nervous system
Hsieh, Y.C., Chiang, M.C., Huang, Y.C., Yeh, T.H., Shih, H.Y., Liu, H.F., Chen, H.Y., Wang, C.P., Cheng, Y.C.
|Source:||Developmental dynamics : an official publication of the American Association of Anatomists 247(12): 1264-1275 (Journal)|
|Keywords:||Pparα, glial precursor, neural development, neuronal precursor, zebrafish|
|PubMed:||30358936 Full text @ Dev. Dyn.|
Hsieh, Y.C., Chiang, M.C., Huang, Y.C., Yeh, T.H., Shih, H.Y., Liu, H.F., Chen, H.Y., Wang, C.P., Cheng, Y.C. (2018) Pparα deficiency inhibits the proliferation of neuronal and glial precursors in the zebrafish central nervous system. Developmental dynamics : an official publication of the American Association of Anatomists. 247(12):1264-1275.
Background Many molecules and signaling pathways involved in neural development play a role in neurodegenerative diseases and brain tumor progression. Peroxisome proliferator-activated receptor (PPAR) proteins regulate the differentiation of tissues and the progression of many diseases. However, the role of these proteins in neural development is unclear.
Results We examined the function of Pparα in the neural development of zebrafish. Two duplicate paralogs for mammalian PPARA/Ppara, namely pparaa and pparab, are present in the zebrafish genome. Both pparaa and pparab are expressed in the developing central nervous system in zebrafish embryos. Inhibiting the function of Pparα by using either the PPARα/Pparα antagonist GW6471 or pparaa or pparab truncated constructs produced identical phenotypes, which were sufficient to reduce the proliferation of neuronal and glial precursor cells without affecting the formation of neural progenitors.
Conclusions We demonstrated that both Pparαa and Pparαb proteins are essential regulators of the proliferation of neuronal and glial precursors. This study provides a better understanding of the functions of PPARα/Pparα in neural development and further expands our knowledge of the potential role of PPARα/Pparα in neurological disorders and brain tumors. This article is protected by copyright. All rights reserved.