Ependyma in Neurodegenerative Diseases, Radiation-Induced Brain Injury and as a Therapeutic Target for Neurotrophic Factors

Author:

Ma Xin-Yu1,Yang Ting-Ting1,Liu Lian2ORCID,Peng Xiao-Chun3,Qian Feng1ORCID,Tang Feng-Ru4

Affiliation:

1. Department of Physiology, School of Basic Medicine, Health Science Center, Yangtze University, Jingzhou 434023, China

2. Department of Pharmacology, School of Basic Medicine, Health Science Center, Yangtze University, Jingzhou 434023, China

3. Department of Pathophysiology, School of Basic Medicine, Health Science Center, Yangtze University, Jingzhou 434023, China

4. Radiation Physiology Laboratory, Singapore Nuclear Research and Safety Initiative, National University of Singapore, Singapore 138602, Singapore

Abstract

The neuron loss caused by the progressive damage to the nervous system is proposed to be the main pathogenesis of neurodegenerative diseases. Ependyma is a layer of ciliated ependymal cells that participates in the formation of the brain-cerebrospinal fluid barrier (BCB). It functions to promotes the circulation of cerebrospinal fluid (CSF) and the material exchange between CSF and brain interstitial fluid. Radiation-induced brain injury (RIBI) shows obvious impairments of the blood–brain barrier (BBB). In the neuroinflammatory processes after acute brain injury, a large amount of complement proteins and infiltrated immune cells are circulated in the CSF to resist brain damage and promote substance exchange through the BCB. However, as the protective barrier lining the brain ventricles, the ependyma is extremely vulnerable to cytotoxic and cytolytic immune responses. When the ependyma is damaged, the integrity of BCB is destroyed, and the CSF flow and material exchange is affected, leading to brain microenvironment imbalance, which plays a vital role in the pathogenesis of neurodegenerative diseases. Epidermal growth factor (EGF) and other neurotrophic factors promote the differentiation and maturation of ependymal cells to maintain the integrity of the ependyma and the activity of ependymal cilia, and may have therapeutic potential in restoring the homeostasis of the brain microenvironment after RIBI or during the pathogenesis of neurodegenerative diseases.

Funder

Jingzhou Science and Technology Department

Health Commission of Hubei Province

National Research Foundation of Singapore to Singapore Nuclear Research and Safety Initiative

Publisher

MDPI AG

Subject

Molecular Biology,Biochemistry

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