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Human FGF1 promoter is active in ependymal cells and dopaminergic neurons in the brains of F1B‐GFP transgenic mice
Author(s) -
Chen MeiShu,
Lin HuaKuo,
Chiu Hsun,
Lee DonChing,
Chung YuFen,
Chiu IngMing
Publication year - 2015
Publication title -
developmental neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.716
H-Index - 129
eISSN - 1932-846X
pISSN - 1932-8451
DOI - 10.1002/dneu.22225
Subject(s) - biology , green fluorescent protein , microbiology and biotechnology , transgene , population , genetically modified mouse , dopaminergic , ependymal cell , neuroscience , gene , central nervous system , genetics , dopamine , demography , sociology
FGF1 is involved in multiple biological functions and exhibits the importance in neuroprotective effects. Our previous studies indicated that, in human brain and retina, the FGF1B promoter controlled the expression of FGF1. However, the exact function and regulation of FGF1 in brain is still unclear. Here, we generated F1B‐GFP transgenic mice that expressed the GFP reporter gene under the control of human FGF1B promoter (−540 to +31). Using the fresh brain sections of F1B‐GFP transgenic mice, we found that the F1B‐GFP cells expressed strong fluorescent signals in the ventricular system throughout the brain. The results of immunohistochemistry further showed that two distinct populations of F1B‐GFP + cells existed in the brains of F1B‐GFP transgenic mice. We demonstrated that one population of F1B‐GFP + cells was ependymal cells, which distributed along the entire ventricles, and the second population of F1B‐GFP + cells was neuronal cells that projected their long processes into multiple directions in specific areas of the brain. The double labeling of F1B‐GFP + cells and tyrosine hydroxylase indicated that a subpopulation of F1B‐GFP + ‐neuronal cells was dopaminergic neurons. Importantly, these F1B‐GFP + /TH + cells were distributed in the main dopaminergic neuronal groups including hypothalamus, ventral tegmental area, and raphe nuclei. These results suggested that human FGF1B promoter was active in ependymal cells, neurons, and a portion of dopaminergic neurons. Thus, the F1B‐GFP transgenic mice provide an animal model not only for studying FGF1 gene expression in vivo but also for understanding the role of FGF1 contribution in neurodegenerative disorders such as Parkinson's disease and Alzheimer's disease. © 2014 Wiley Periodicals, Inc. Develop Neurobiol 75: 232–248, 2015

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