Microarray Analysis of Gene Expression Changes in Neuroplastin 65-Knockout Mice: Implications for Abnormal Cognition and Emotional Disorders.
10.1007/s12264-018-0251-5
- Author:
Huanhuan LI
1
;
Jiujiang ZENG
1
;
Liang HUANG
1
;
Dandan WU
1
;
Lifen LIU
1
;
Yutong LIU
2
;
Qionglan YUAN
3
Author Information
1. Department of Neurology, Shanghai Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, China.
2. Department of Radiology, University of Nebraska Medical Center, Omaha, NE, 68198, USA.
3. Department of Neurology, Shanghai Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, China. yqiongl@tongji.edu.cn.
- Publication Type:Journal Article
- Keywords:
Gene expression profile;
Htr3a;
Microarray analysis;
Neuroplastin 65;
Wnt
- MeSH:
Affective Symptoms;
metabolism;
Animals;
Brain;
diagnostic imaging;
metabolism;
pathology;
Cognition Disorders;
metabolism;
Gene Expression;
Magnetic Resonance Imaging;
Membrane Glycoproteins;
deficiency;
genetics;
physiology;
Mice, Knockout;
Microarray Analysis;
Organ Size;
Real-Time Polymerase Chain Reaction;
Wnt3 Protein;
metabolism
- From:
Neuroscience Bulletin
2018;34(5):779-788
- CountryChina
- Language:English
-
Abstract:
Neuroplastin 65 (Np65) is an immunoglobulin superfamily cell adhesion molecule involved in synaptic formation and plasticity. Our recent study showed that Np65-knockout (KO) mice exhibit abnormal cognition and emotional disorders. However, the underlying mechanisms remain unclear. In this study, we found 588 differentially-expressed genes in Np65-KO mice by microarray analysis. RT-PCR analysis also revealed the altered expression of genes associated with development and synaptic structure, such as Cdh1, Htr3a, and Kcnj9. In addition, the expression of Wnt-3, a Wnt protein involved in development, was decreased in Np65-KO mice as evidenced by western blotting. Surprisingly, MRI and DAPI staining showed a significant reduction in the lateral ventricular volume of Np65-KO mice. Together, these findings suggest that ablation of Np65 influences gene expression, which may contribute to abnormal brain development. These results provide clues to the mechanisms underlying the altered brain functions of Np65-deficient mice.
