Piezo channel plays a part in retinal ganglion cell damage.


Journal

Experimental eye research
ISSN: 1096-0007
Titre abrégé: Exp Eye Res
Pays: England
ID NLM: 0370707

Informations de publication

Date de publication:
02 2020
Historique:
received: 18 09 2019
revised: 27 11 2019
accepted: 20 12 2019
pubmed: 25 12 2019
medline: 25 7 2020
entrez: 25 12 2019
Statut: ppublish

Résumé

Piezo channel is one of the mechanosensitive channels that senses pressure and shearing stress. Previous reports show that Piezo channel is expressed in many tissues such as skin and lung and they have many important roles. In addition, the mRNA of Piezo has been detected in astrocytes in the optic nerve head of mice. However, it is not yet clear where Piezo channel localize in eye and what kind of effects it have. Thus, the purpose of this study was to determine the expression sites of Piezo channel in mouse eyes and effect of Piezo channel on retinal ganglion cells. Immunostaining analysis showed that the Piezo 1/2 were expressed in the cornea, trabecular meshwork of the anterior ocular segment, lens epithelial cells, and on the retinal ganglion cell layer. The expression of retinal Piezo 2 was increased in retinal disorder model mouse caused by high IOP. Piezo 1 agonist Yoda 1 suppressed neurite outgrowth in retinal ganglion cells. On the other hand, Piezo antagonist GsMTx4 promoted neurite outgrowth in retinal ganglion cells. These findings indicate that Piezo channel may contribute to diseases relating the IOP such as glaucoma.

Identifiants

pubmed: 31874142
pii: S0014-4835(19)30703-1
doi: 10.1016/j.exer.2019.107900
pii:
doi:

Substances chimiques

Intercellular Signaling Peptides and Proteins 0
Ion Channels 0
MTx4 protein, Grammostola spatulata 0
Piezo1 protein, mouse 0
Piezo2 protein, mouse 0
Pyrazines 0
Spider Venoms 0
Thiadiazoles 0
yoda-1 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

107900

Informations de copyright

Copyright © 2019 Elsevier Ltd. All rights reserved.

Auteurs

Wataru Morozumi (W)

Molecular Pharmacology, Department of Biofunctional Evaluation, Gifu Pharmaceutical University, Gifu, Japan.

Satoshi Inagaki (S)

Molecular Pharmacology, Department of Biofunctional Evaluation, Gifu Pharmaceutical University, Gifu, Japan.

Yuki Iwata (Y)

Molecular Pharmacology, Department of Biofunctional Evaluation, Gifu Pharmaceutical University, Gifu, Japan.

Shinsuke Nakamura (S)

Molecular Pharmacology, Department of Biofunctional Evaluation, Gifu Pharmaceutical University, Gifu, Japan.

Hideaki Hara (H)

Molecular Pharmacology, Department of Biofunctional Evaluation, Gifu Pharmaceutical University, Gifu, Japan.

Masamitsu Shimazawa (M)

Molecular Pharmacology, Department of Biofunctional Evaluation, Gifu Pharmaceutical University, Gifu, Japan. Electronic address: shimazawa@gifu-pu.ac.jp.

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Classifications MeSH