Time course of collateral vessel formation after retinal vein occlusion visualized by OCTA and elucidation of factors in their formation.
Collateral vessels
OCTA
RVO
Journal
Heliyon
ISSN: 2405-8440
Titre abrégé: Heliyon
Pays: England
ID NLM: 101672560
Informations de publication
Date de publication:
Jan 2021
Jan 2021
Historique:
received:
28
08
2020
revised:
01
12
2020
accepted:
31
12
2020
entrez:
21
1
2021
pubmed:
22
1
2021
medline:
22
1
2021
Statut:
epublish
Résumé
It is clinically recognized that collateral vessels can form after retinal vein occlusion (RVO) in some cases and these vessels can lead to spontaneous recovery of the pathological condition. In recent years, optical coherence tomography angiography (OCTA) has become a decisive clinical instrument. Unlike previous angiography tests, OCTA enables the non-invasive visualization of fundus vasculature without the need for administration of a contrast agent. However, it remains to be determined if OCTA depicts the 'true' histological status as several studies have reported artifacts in OCTA imaging. We generated a laser-induced mouse RVO model, and evaluated the subsequent formation of collateral vessels in order to understand the mechanisms by which collateral vessels form using OCTA imaging, as well as molecular and histological assessments. We succeeded in visualizing the time course of collateral vessel formation in a mouse RVO model and confirmed the similarity in formation of collateral vessels only within the deep layer of the retina in both human and mouse. We hypothesized that sphingosine 1-phosphate receptor-1 (S1PR1) may play important roles via vascular shear stress linking vein occlusion and collateral vessel formation. Results from OCTA revealed that collateral vessels are increased in response to administration of a S1PR1 agonist in a mouse RVO model. Based on quantitative reverse transcription polymerase chain reaction (qRT-PCR), S1PR1 messenger ribonucleic acid (mRNA) levels in the whole retina peaked 6 h after photocoagulation in this model. Immunohistochemical staining of retinal flat mounts revealed that S1PR1 staining occurred along the laser-occluded blood vessels. We observed the temporal process of collateral vessel formation in a mouse RVO model and identified the relationship between S1PR1 and shear stress as one of the factors in collateral vessel formation in RVO.
Sections du résumé
BACKGROUND
BACKGROUND
It is clinically recognized that collateral vessels can form after retinal vein occlusion (RVO) in some cases and these vessels can lead to spontaneous recovery of the pathological condition. In recent years, optical coherence tomography angiography (OCTA) has become a decisive clinical instrument. Unlike previous angiography tests, OCTA enables the non-invasive visualization of fundus vasculature without the need for administration of a contrast agent. However, it remains to be determined if OCTA depicts the 'true' histological status as several studies have reported artifacts in OCTA imaging.
METHODS
METHODS
We generated a laser-induced mouse RVO model, and evaluated the subsequent formation of collateral vessels in order to understand the mechanisms by which collateral vessels form using OCTA imaging, as well as molecular and histological assessments.
RESULTS
RESULTS
We succeeded in visualizing the time course of collateral vessel formation in a mouse RVO model and confirmed the similarity in formation of collateral vessels only within the deep layer of the retina in both human and mouse. We hypothesized that sphingosine 1-phosphate receptor-1 (S1PR1) may play important roles via vascular shear stress linking vein occlusion and collateral vessel formation. Results from OCTA revealed that collateral vessels are increased in response to administration of a S1PR1 agonist in a mouse RVO model. Based on quantitative reverse transcription polymerase chain reaction (qRT-PCR), S1PR1 messenger ribonucleic acid (mRNA) levels in the whole retina peaked 6 h after photocoagulation in this model. Immunohistochemical staining of retinal flat mounts revealed that S1PR1 staining occurred along the laser-occluded blood vessels.
CONCLUSION
CONCLUSIONS
We observed the temporal process of collateral vessel formation in a mouse RVO model and identified the relationship between S1PR1 and shear stress as one of the factors in collateral vessel formation in RVO.
Identifiants
pubmed: 33474512
doi: 10.1016/j.heliyon.2021.e05902
pii: S2405-8440(21)00007-4
pmc: PMC7803649
doi:
Types de publication
Journal Article
Langues
eng
Pagination
e05902Informations de copyright
© 2021 The Authors.
Déclaration de conflit d'intérêts
The authors declare no conflict of interest.
Références
Jpn J Ophthalmol. 2007 Jul-Aug;51(4):251-7
pubmed: 17660984
Sci Rep. 2016 Jul 08;6:29445
pubmed: 27389770
Br J Ophthalmol. 2019 Oct;103(10):1373-1379
pubmed: 30467130
Neural Regen Res. 2016 Mar;11(3):368-71
pubmed: 27127459
Am J Ophthalmol. 2016 Jan;161:126-32.e1
pubmed: 26454243
Ophthalmol Retina. 2019 Sep;3(9):767-776
pubmed: 31167729
Cell J. 2020 Jan;21(4):479-493
pubmed: 31376330
Arterioscler Thromb Vasc Biol. 2015 Feb;35(2):348-57
pubmed: 25425620
Ophthalmology. 1999 Nov;106(11):2054-62
pubmed: 10571337
PLoS One. 2015 Mar 16;10(3):e0119046
pubmed: 25775456
Invest Ophthalmol Vis Sci. 2017 Dec 1;58(14):6175-6192
pubmed: 29222552
Nat Med. 2004 May;10(5):502-9
pubmed: 15098027
Cells. 2019 Apr 27;8(5):
pubmed: 31035633
Int J Retina Vitreous. 2015 Apr 15;1:5
pubmed: 27847598
Invest Ophthalmol Vis Sci. 2020 Feb 7;61(2):34
pubmed: 32084269
PLoS One. 2019 Jul 24;14(7):e0215790
pubmed: 31339897
J Invasive Cardiol. 2019 Mar;31(3):49-51
pubmed: 30819974
PLoS One. 2018 Aug 9;13(8):e0201958
pubmed: 30092067
Sci Rep. 2017 Mar 02;7:43509
pubmed: 28252108
Retina. 2015 Nov;35(11):2347-52
pubmed: 26469532
J Bone Miner Res. 2018 Nov;33(11):2035-2047
pubmed: 29949664
Prog Retin Eye Res. 2018 May;64:1-55
pubmed: 29229445
J Stroke Cerebrovasc Dis. 2018 May;27(5):1237-1251
pubmed: 29337049
PLoS One. 2015 Sep 14;10(9):e0138029
pubmed: 26367258
Int J Ophthalmol. 2014 Apr 18;7(2):232-8
pubmed: 24790863
JAMA Ophthalmol. 2018 Nov 1;136(11):1262-1270
pubmed: 30352115