PuSH - Publication Server of Helmholtz Zentrum München: HDAC inhibition in the <em>cpfl1</em> mouse protects degenerating cone photoreceptors <em>in vivo</em>.

Information

Clues to quality of journals

Open Access Policy of Helmholtz Association 2016

CC Licencences

Publication Metrics

Navigation

Home

Deutsch

EVA: Electronic Publishing

New EVA Application

Research

Advanced Search

Browse by ...

... HMGU-Authors/Consortia

... Organizational Structure

... Journal

... Publication Type

... Research Data

... Arbeitsgruppen

... Publication Year

Publication overview

Statistics

Statistics (last 5 years)

OA Publications

Publish

Submit Publication

Import publication from...

...EVA

Report missing publication

Highlights

Support & Contact

Contact persons

Help

Data protection

Helmholtz Open Science

JANE Journal Estimator

SHERPA/RoMEO

DOAJ

Export:

Text

Endnote (RIS) BIB

BibTeX

Trifunovic, D.* ; Arango-González, B.* ; Comitato, A.* ; Barth, M.* ; del Amo, E.M.* ; Kulkarni, M.* ; Sahaboglu, A.* ; Hauck, S.M. ; Urtti, A.* ; Arsenijevic, Y.* ; Ueffing, M.* ; Marigo, V.* ; Paquet-Durand, F.*

HDAC inhibition in the cpfl1 mouse protects degenerating cone photoreceptors in vivo.

Hum. Mol. Genet. 25, 4462-4472 (2016)

Publ. Version/Full Text

Postprint

Supplement

DOI

PMC

	Open Access Green

Abstract
Metrics
Extra information

Cone photoreceptor cell death as it occurs in certain hereditary retinal diseases is devastating, with the affected patients suffering from a loss of accurate and color vision. Regrettably, these hereditary cone diseases are still untreatable to date. Thus, the identification of substances able to block or restrain cone cell death is of primary importance. We studied the neuroprotective effects of a histone deacetylase inhibitor, Trichostatin A (TSA), in a mouse model of inherited, primary cone degeneration (cpfl1). We show that HDAC inhibition protects cpfl1 cones in vitro, in retinal explant cultures. More importantly, in vivo, a single intravitreal TSA injection significantly increased cone survival for up to 16 days post-injection. In addition, the abnormal, incomplete cone migration pattern in the cpfl1 retina was significantly improved by HDAC inhibition. These findings suggest a crucial role for HDAC activity in primary cone degeneration and highlight a new avenue for future therapy developments for cone dystrophies and retinal diseases associated with impaired cone migration.

Impact Factor

Scopus SNIP

Web of Science
Times Cited

Scopus
Cited By

Altmetric

5.985

1.327