Cytoglobin deficiency potentiates Crb1-mediated retinal degeneration in rd8 mice.
Animals
Cytoglobin
/ genetics
Disease Models, Animal
Eye Proteins
/ genetics
Female
Homozygote
Male
Membrane Proteins
/ metabolism
Mice
Mice, Inbred C57BL
Mice, Knockout
Mutation
Nerve Tissue Proteins
/ genetics
Phenotype
Retina
/ metabolism
Retinal Degeneration
/ genetics
Retinal Ganglion Cells
/ metabolism
Journal
Developmental biology
ISSN: 1095-564X
Titre abrégé: Dev Biol
Pays: United States
ID NLM: 0372762
Informations de publication
Date de publication:
15 02 2020
15 02 2020
Historique:
received:
29
01
2019
revised:
15
10
2019
accepted:
16
10
2019
pubmed:
22
10
2019
medline:
2
9
2020
entrez:
22
10
2019
Statut:
ppublish
Résumé
The purpose of this study is to determine the effect of Cytoglobin (Cygb) deficiency on Crb1-related retinopathy. The Crb1 cell polarity complex is required for photoreceptor function and survival. Crb1-related retinopathies encompass a broad range of phenotypes which are not completely explained by the variability of Crb1 mutations. Genes thought to modify Crb1 function are therefore important targets of research. The biological function of Cygb involves oxygen delivery, scavenging of reactive oxygen species, and nitric oxide metabolism. However, the relationship of Cygb to diseases involving the Crb1 cell polarity complex is unknown. Cygb knockout mice homozygous for the rd8 mutation (Cygb Cygb Cygb is necessary for retinal lamination, maintenance of cell polarity, and photoreceptor survival in rd8 mice. These results are consistent with Cygb as a disease modifying gene in Crb1-related retinopathy. Further studies are necessary to investigate the role of Cygb in the human retina.
Identifiants
pubmed: 31634437
pii: S0012-1606(19)30055-7
doi: 10.1016/j.ydbio.2019.10.013
pmc: PMC6995765
mid: NIHMS1542952
pii:
doi:
Substances chimiques
Crb1 protein, mouse
0
Cygb protein, mouse
0
Cytoglobin
0
Eye Proteins
0
Membrane Proteins
0
Nerve Tissue Proteins
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
141-152Subventions
Organisme : NEI NIH HHS
ID : K08 EY027463
Pays : United States
Organisme : NEI NIH HHS
ID : P30 EY012576
Pays : United States
Organisme : NEI NIH HHS
ID : R01 EY019497
Pays : United States
Organisme : NIH HHS
ID : UM1 OD023221
Pays : United States
Informations de copyright
Copyright © 2019 Elsevier Inc. All rights reserved.
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