Retinal ganglion cell loss in kinesin-1 cargo Alcadein α deficient mice.
Adaptor Proteins, Signal Transducing
/ metabolism
Animals
Axonal Transport
/ physiology
Axons
/ metabolism
Disease Models, Animal
Intraocular Pressure
/ physiology
Kinesins
/ deficiency
Low Tension Glaucoma
/ metabolism
Mice, Knockout
Retina
/ metabolism
Retinal Ganglion Cells
/ metabolism
Transport Vesicles
/ metabolism
Journal
Cell death & disease
ISSN: 2041-4889
Titre abrégé: Cell Death Dis
Pays: England
ID NLM: 101524092
Informations de publication
Date de publication:
03 03 2020
03 03 2020
Historique:
received:
09
12
2019
accepted:
20
02
2020
revised:
11
02
2020
entrez:
5
3
2020
pubmed:
5
3
2020
medline:
10
4
2021
Statut:
epublish
Résumé
Maintenance of retinal ganglion cells (RGCs) activity is relied on axonal transport conveying materials required for their survival such as neurotrophic factors. Kinesin-1 undergoes anterograde transport in axons, and Alcadein α (Alcα; also called calsyntenin-1) is a major cargo adaptor protein that can drive kinesin-1 to transport vesicles containing Alcα. The long-term effects of Alcα-deficiency on retinal morphology and survival of RGCs during postnatal development were examined in Alcα knockout mice. At 1.5, 3, 6, and 15 months postnatal, the number of retrogradely labeled RGCs was determined in flat-mounted retinas of Alcα-deficient and wild-type mice. Retinal damage was assessed histologically by determining the retinal thickness. Intraocular pressure (IOP) was measured with a Tonolab tonometer. At 1.5 months postnatal, the number of retrogradely labeled RGCs was not different between wild-type and Alcα-deficient mice. However, at 3, 6, and 15 months postnatal, the number of RGCs was significantly lower in Alcα deficient mice than those of wild-type mice (143 ± 41.1 cells/mm
Identifiants
pubmed: 32127528
doi: 10.1038/s41419-020-2363-x
pii: 10.1038/s41419-020-2363-x
pmc: PMC7054276
doi:
Substances chimiques
Adaptor Proteins, Signal Transducing
0
Kinesins
EC 3.6.4.4
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
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