Primary cilia are present on endothelial cells of the hyaloid vasculature but are not required for the development of the blood-retinal barrier.


Journal

PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081

Informations de publication

Date de publication:
2020
Historique:
received: 31 10 2019
accepted: 14 07 2020
entrez: 1 8 2020
pubmed: 1 8 2020
medline: 5 9 2020
Statut: epublish

Résumé

Endothelial cilia are found in a variety of tissues including the cranial vasculature of zebrafish embryos. Recently, endothelial cells in the developing mouse retina were reported to also possess primary cilia that are potentially involved in vascular remodeling. Fish carrying mutations in intraflagellar transport (ift) genes have disrupted cilia and have been reported to have an increased rate of spontaneous intracranial hemorrhage (ICH), potentially due to disruption of the sonic hedgehog (shh) signaling pathway. However, it remains unknown whether the endothelial cells forming the retinal microvasculature in zebrafish also possess cilia, and whether endothelial cilia are necessary for development and maintenance of the blood-retinal barrier (BRB). In the present study, we found that the endothelial cells lining the zebrafish hyaloid vasculature possess primary cilia during development. To determine whether endothelial cilia are necessary for BRB integrity, ift57, ift88, and ift172 mutants, which lack cilia, were crossed with the double-transgenic zebrafish strain Tg(l-fabp:DBP-EGFP;flk1:mCherry). This strain expresses a vitamin D-binding protein (DBP) fused to enhanced green fluorescent protein (EGFP) as a tracer in the blood plasma, while the endothelial cells forming the vasculature are tagged by mCherry. The Ift mutant fish develop a functional BRB, indicating that endothelial cilia are not necessary for early BRB integrity. Additionally, although treatment of zebrafish larvae with Shh inhibitor cyclopamine results in BRB breakdown, the Ift mutant fish were not sensitized to cyclopamine-induced BRB breakdown.

Identifiants

pubmed: 32735563
doi: 10.1371/journal.pone.0225351
pii: PONE-D-19-30359
pmc: PMC7394433
doi:

Substances chimiques

Adaptor Proteins, Signal Transducing 0
Hedgehog Proteins 0
IFT57 protein, zebrafish 0
Veratrum Alkaloids 0
Zebrafish Proteins 0
cyclopamine ZH658AJ192

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e0225351

Subventions

Organisme : NEI NIH HHS
ID : P30 EY025585
Pays : United States
Organisme : NEI NIH HHS
ID : R01 EY026181
Pays : United States
Organisme : NEI NIH HHS
ID : R01 EY027083
Pays : United States
Organisme : NEI NIH HHS
ID : T32 EY024236
Pays : United States

Déclaration de conflit d'intérêts

The authors have declared that no competing interests exist.

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Auteurs

Lana M Pollock (LM)

Department of Ophthalmic Research, Cole Eye Institute, Cleveland Clinic, Cleveland, OH, United States of America.

Brian Perkins (B)

Department of Ophthalmic Research, Cole Eye Institute, Cleveland Clinic, Cleveland, OH, United States of America.
Department of Ophthalmology, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH, United States of America.

Bela Anand-Apte (B)

Department of Ophthalmic Research, Cole Eye Institute, Cleveland Clinic, Cleveland, OH, United States of America.
Department of Ophthalmology, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH, United States of America.

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Classifications MeSH