Cellular senescence mediates retinal ganglion cell survival regulation post-optic nerve crush injury.
Journal
Cell proliferation
ISSN: 1365-2184
Titre abrégé: Cell Prolif
Pays: England
ID NLM: 9105195
Informations de publication
Date de publication:
18 Jul 2024
18 Jul 2024
Historique:
revised:
24
06
2024
received:
25
05
2024
accepted:
08
07
2024
medline:
18
7
2024
pubmed:
18
7
2024
entrez:
18
7
2024
Statut:
aheadofprint
Résumé
Traumatic optic neuropathy refers to optic nerve (ON) injury by trauma, including explosion and traffic accident. Retinal ganglion cell (RGC) death is the critical pathological cause of irreversible visual impairment and blindness in ON injury. We previously investigated the patterns of 11 modes of cell death in mouse retina post-ON injury. Here we aimed to identify additional signalling pathways regulating RGC survival in rodents post-ON injury. RNA sequencing analysis identified the upregulation of inflammation and cellular senescence-related genes in retina post-ON injury, which were confirmed by immunoblotting and immunofluorescence analyses. Increased expression of senescence-associated β-galactosidase (SA-βgal) in RGCs and activation of microglia were also found. Transforming growth factor-β receptor type II inhibitor (LY2109761) treatment suppressed p15
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e13719Subventions
Organisme : Natural Science Foundation of Guangdong Province
ID : 2023A1515010195
Organisme : National Natural Science Foundation of China
ID : 82371049
Informations de copyright
© 2024 The Author(s). Cell Proliferation published by Beijing Institute for Stem Cell and Regenerative Medicine and John Wiley & Sons Ltd.
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