ArticleInvestigative ophthalmology & visual science2014
Pulmonary surfactant protein a is expressed in mouse retina by Müller cells and impacts neovascularization in oxygen-induced retinopathy.
Article in Investigative ophthalmology & visual science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Surfactant proteins A and D nucleotide variants: association with retinal vascular disease.Pediatric research · 2026Article
- Research article expression of surfactant protein-A and D, and CD9 in lungs of 1 and 30 day old foals.BMC veterinary research · 2021Article
- Article
- Surfactant protein A is expressed in the central nervous system of rats with experimental autoimmune encephalomyelitis, and suppresses inflammation in human astrocytes and microglia.Molecular medicine reports · 2017Article
- Structure, genetics and function of the pulmonary associated surfactant proteins A and D: The extra-pulmonary role of these C type lectins.Annals of anatomy = Anatomischer Anzeiger : official organ of the Anatomische Gesellschaft · 2017Review
- Article
- The role of Toll-like receptors in retinal ischemic diseases.International journal of ophthalmology · 2016Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
purposeSurfactant protein A (SP-A) up-regulates cytokine expression in lung disease of prematurity. Here we present data that for the first time characterizes SP-A expression and localization in the mouse retina and its impact on neovascularization (NV) in the mouse.
methodsRetinal SP-A was localized in wild-type (WT) mice with the cell markers glutamine synthetase (Müller cells), neurofilament-M (ganglion cells), glial acid fibrillary acid protein (astrocytes), and cluster of differentiation 31 (endothelial cells). Toll-like receptor 2 and 4 (TLR-2 and TLR-4) ligands were used to up-regulate SP-A expression in WT and myeloid differentiation primary response 88 (MyD88) protein (necessary for NFκB signaling) null mouse retinas and Müller cells, which were quantified using ELISA. Retinal SP-A was then measured in the oxygen-induced retinopathy (OIR) mouse model. The effect of SP-A on retinal NV was then studied in SP-A null (SP-A(-/-)) mice.
resultsSP-A is present at birth in the WT mouse retina and colocalizes with glutamine synthetase. TLR-2 and TLR-4 ligands increase SP-A both in the retina and in Müller cells. SP-A is increased at postnatal day 17 (P17) in WT mouse pups with OIR compared to that in controls (P = 0.02), and SP-A(-/-) mice have reduced NV compared to WT mice (P = 0.001) in the OIR model.
conclusionsRetinal and Müller cell SP-A is up-regulated via the NFκB pathway and up-regulated during the hypoxia phase of OIR. Absence of SP-A attenuates NV in the OIR model. Thus SP-A may be a marker of retinal inflammation during NV.
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