Decrease in the T-box1 gene expression in embryonic brain and adult hippocampus of down syndrome mouse models

被引:2
作者
Shimizu, Ryohei [1 ]
Ishihara, Keiichi [1 ]
Kawashita, Eri [1 ]
Sago, Haruhiko [2 ]
Yamakawa, Kazuhiro [3 ]
Mizutani, Ken-ichi [4 ]
Akiba, Satoshi [1 ]
机构
[1] Kyoto Pharmaceut Univ, Dept Pathol Biochem, Div Pathol Sci, Kyoto 6078414, Japan
[2] Natl Ctr Child Hlth & Dev, Ctr Maternal Fetal Neonatal & Reprod Med, Tokyo 1578535, Japan
[3] Nagoya City Univ, Inst Brain Sci, Dept Neurodev Disorder Genet, Grad Sch Med Sci, Nagoya, Aichi 4678601, Japan
[4] Kobe Gakuin Univ, Grad Sch Pharmaceut Sci, Lab Stem Cell Biol, Kobe, Hyogo 6508586, Japan
关键词
Down syndrome; Mouse models; Transcriptomics; Tbx1; Fetal brain; Adult hippocampus; TS1CJE; REGION; FETUSES; PROLIFERATION; NEUROGENESIS; PHENOTYPES; NUMBER; TS65DN; MICE;
D O I
10.1016/j.bbrc.2020.12.026
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Down syndrome (DS, Trisomy 21) is the most common genetic cause of delayed fetal brain development and postnatal intellectual disability. Although delayed fetal brain development might be involved in intellectual disability, no evidence of an association between these abnormal phenotypes has been shown. To identify molecules differentially expressed in both the prenatal forebrain and adult hippocampus of Ts1Cje mice, a mouse model of DS, we employed a transcriptomic analysis. In the present study, we conducted transcriptomic profiling of the hippocampus of adult Ts1Cje mice and compared the results with the previously obtained transcriptomic profile of the prenatal forebrain at embryonic day 14.5. Results showed that the Tbx1 mRNA expression was decreased at both life stages. In addition, the decreased expression of Tbx1 mRNA was confirmed in other DS mouse models, Dp(16)1Yey/+ and Ts1Rhr mice, which carry longer and shorter trisomic regions, respectively. Taken together, these findings suggest that Tbxl may link the delayed fetal brain development and intellectual disability in DS. (C) 2020 Elsevier Inc. All rights reserved.
引用
收藏
页码:87 / 92
页数:6
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