UM  > 中華醫藥研究院
Alterations in AQP4 expression and polarization in the course of motor neuron degeneration in SOD1G93A mice
Dai, Jiaying1; Lin, Weihao2; Zheng, Minying1; Liu, Qiang3; He, Baixuan1; Luo, Chuanming3; Lu, Xilin1; Pei, Zhong1; Su, Huanxing3; Yao, Xiaoli1
2017-08
Source PublicationMOLECULAR MEDICINE REPORTS
ISSN1791-2997
Volume16Issue:2Pages:1739-1746
Abstract

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterized by selective degeneration of upper and lower motor neurons. The disease progression is associated with the astrocytic environment. Aquaporin-4 (AQP4) water channels are the most abundant AQPs expressed in astrocytes, exerting important influences on central nervous system homeostasis. The present study aimed to characterize the alterations in AQP4 expression and localization in superoxide dismutase 1 (SOD1) G93A transgenic mice. SOD1G93A mice were sacrificed during the presymptomatic, disease onset and end stages and immunostaining was performed on spinal cord sections to investigate neuronal loss, glial activation and AQP4 expression in the spinal cord. It was observed that global AQP4 expression increased in the spinal cord of SOD1G93A mice as the disease progressed. However, AQP4 polarization decreased as the disease progressed, and AQP4 polarized localization at the endfeet of astrocytes was decreased in the spinal ventral horn of SOD1G93A mice at the disease onset and end stages. Meanwhile, motor neuron degeneration and decreased glutamate transporter 1 expression in astrocytes in SOD1G93A mice were observed as the disease progressed. The results of the present study demonstrated that AQP4 depolarization is a widespread pathological condition and may contribute to motor neuron degeneration in ALS.

KeywordAmyotrophic Lateral Sclerosis Astrocyte Aquaporin-4 Polarization Glutamate Transporter 1 Superoxide Dismutase 1 G93a Mice
DOI10.3892/mmr.2017.6786
URLView the original
Indexed BySCI
Language英语
WOS Research AreaOncology ; Research & Experimental Medicine
WOS SubjectOncology ; Medicine, Research & Experimental
WOS IDWOS:000405079300100
PublisherSPANDIDOS PUBL LTD
The Source to ArticleWOS
Fulltext Access
Citation statistics
Cited Times [WOS]:4   [WOS Record]     [Related Records in WOS]
Document TypeJournal article
CollectionInstitute of Chinese Medical Sciences
Corresponding AuthorSu, Huanxing; Yao, Xiaoli
Affiliation1.Department of Neurology, National Key Clinical Department and Key Discipline of Neurology
2.Department of Breast and Thyroid Surgery, The First Affiliated Hospital, Sun Yat‑sen University, Guangzhou, Guangdong 510080
3.State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macau SAR 999078, P.R. China
Corresponding Author AffilicationInstitute of Chinese Medical Sciences
Recommended Citation
GB/T 7714
Dai, Jiaying,Lin, Weihao,Zheng, Minying,et al. Alterations in AQP4 expression and polarization in the course of motor neuron degeneration in SOD1G93A mice[J]. MOLECULAR MEDICINE REPORTS,2017,16(2):1739-1746.
APA Dai, Jiaying.,Lin, Weihao.,Zheng, Minying.,Liu, Qiang.,He, Baixuan.,...&Yao, Xiaoli.(2017).Alterations in AQP4 expression and polarization in the course of motor neuron degeneration in SOD1G93A mice.MOLECULAR MEDICINE REPORTS,16(2),1739-1746.
MLA Dai, Jiaying,et al."Alterations in AQP4 expression and polarization in the course of motor neuron degeneration in SOD1G93A mice".MOLECULAR MEDICINE REPORTS 16.2(2017):1739-1746.
Related Services
Recommend this item
Bookmark
Usage statistics
Export to Endnote
Google Scholar
Similar articles in Google Scholar
[Dai, Jiaying]'s Articles
[Lin, Weihao]'s Articles
[Zheng, Minying]'s Articles
Baidu academic
Similar articles in Baidu academic
[Dai, Jiaying]'s Articles
[Lin, Weihao]'s Articles
[Zheng, Minying]'s Articles
Bing Scholar
Similar articles in Bing Scholar
[Dai, Jiaying]'s Articles
[Lin, Weihao]'s Articles
[Zheng, Minying]'s Articles
Terms of Use
No data!
Social Bookmark/Share
All comments (0)
No comment.
 

Items in the repository are protected by copyright, with all rights reserved, unless otherwise indicated.