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α-Aminoadipic acid protects against retinal disruption through attenuating Müller cell gliosis in a rat model of acute ocular hypertension

Overview of attention for article published in Drug Design, Development and Therapy, October 2016
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Title
α-Aminoadipic acid protects against retinal disruption through attenuating Müller cell gliosis in a rat model of acute ocular hypertension
Published in
Drug Design, Development and Therapy, October 2016
DOI 10.2147/dddt.s105362
Pubmed ID
Authors

Xiaolei Wang, Jier Su, Jingwen Ding, Song Han, Wei Ma, Hong Luo, Guy Hughes, Zhaoyang Meng, Yi Yin, Yanling Wang, Junfa Li

Abstract

Ocular hypertension is an important risk factor for glaucoma. The purpose of this study was to investigate the gliotoxic effects of α-aminoadipic acid (AAA) in a rat model of AOH and its underlying mechanisms. In the rat model of acute ocular hypertension (AOH), intraocular pressure was increased to 110 mmHg for 60 minutes. Animals were divided into four groups: sham operation (Ctrl), AOH, AOH + phosphate-buffered saline (PBS), and AOH + AAA. Cell apoptosis in the ganglion cell layer was detected with the terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end labeling (TUNEL) assay, and retinal ganglion cells (RGCs) immunostained with Thy-1 were counted. Müller cell activation was detected using immunostaining with glutamine synthetase and glial fibrillary acidic protein. Tumor necrosis factor-α (TNF-α) was examined using Western blot. In the rat model of AOH, cell apoptosis was induced in the ganglion cell layer and the number of RGCs was decreased. Müller cell gliosis in the retinas of rats was induced, and retinal protein levels of TNF-α were increased. Intravitreal treatment of AAA versus PBS control attenuated these retinal abnormalities to show protective effects in the rat model of AOH. In the retinas of the rat model of AOH, AAA treatment attenuated retinal apoptosis in the ganglion cell layer and preserved the number of RGCs, likely through the attenuation of Müller cell gliosis and suppression of TNF-α induction. Our observations suggest that AAA might be a potential therapeutic target in glaucoma.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 13 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 13 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 3 23%
Student > Ph. D. Student 2 15%
Other 1 8%
Student > Bachelor 1 8%
Lecturer 1 8%
Other 2 15%
Unknown 3 23%
Readers by discipline Count As %
Neuroscience 4 31%
Biochemistry, Genetics and Molecular Biology 3 23%
Agricultural and Biological Sciences 1 8%
Medicine and Dentistry 1 8%
Computer Science 1 8%
Other 0 0%
Unknown 3 23%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 20 October 2016.
All research outputs
#22,759,452
of 25,374,647 outputs
Outputs from Drug Design, Development and Therapy
#1,754
of 2,268 outputs
Outputs of similar age
#292,213
of 332,576 outputs
Outputs of similar age from Drug Design, Development and Therapy
#44
of 62 outputs
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