Pulmonary surfactant protein a is expressed in mouse retina by müuller cells and impacts neovascularization in oxygen-induced retinopathy

Faizah Bhatti; Genevieve Ball; Ronald Hobbs; Annette Linens; Saad Munzar; Rizwan Akram; Alistair J. Barber; Michael Anderson; Michael Elliott; Madeline Edwards

doi:10.1167/iovs.13-13652

Pulmonary surfactant protein a is expressed in mouse retina by müuller cells and impacts neovascularization in oxygen-induced retinopathy

Faizah Bhatti, Genevieve Ball, Ronald Hobbs, Annette Linens, Saad Munzar, Rizwan Akram, Alistair J. Barber, Michael Anderson, Michael Elliott, Madeline Edwards

Research output: Contribution to journal › Article › peer-review

9 Scopus citations

Abstract

PURPOSE. Surfactant 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.

METHODS. Retinal SP-A was localized in wild-type (WT) mice with the cell markers glutamine synthetase (M¨uller 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 NFjB signaling) null mouse retinas and Müuller 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.

RESULTS. SP-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 Müuller 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.

CONCLUSIONS. Retinal and Müller cell SP-A is up-regulated via the NFjB pathway and upregulated 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.

Original language	English (US)
Pages (from-to)	232-242
Number of pages	11
Journal	Investigative Ophthalmology and Visual Science
Volume	56
Issue number	1
DOIs	https://doi.org/10.1167/iovs.13-13652
State	Published - Nov 18 2015

All Science Journal Classification (ASJC) codes

Ophthalmology
Sensory Systems
Cellular and Molecular Neuroscience

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10.1167/iovs.13-13652

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Bhatti, F., Ball, G., Hobbs, R., Linens, A., Munzar, S., Akram, R., Barber, A. J., Anderson, M., Elliott, M., & Edwards, M. (2015). Pulmonary surfactant protein a is expressed in mouse retina by müuller cells and impacts neovascularization in oxygen-induced retinopathy. Investigative Ophthalmology and Visual Science, 56(1), 232-242. https://doi.org/10.1167/iovs.13-13652

@article{e6f4bd85971d4b6ea0b6e432e8d0ed81,

title = "Pulmonary surfactant protein a is expressed in mouse retina by m{\"u}uller cells and impacts neovascularization in oxygen-induced retinopathy",

abstract = "PURPOSE. Surfactant 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.METHODS. Retinal SP-A was localized in wild-type (WT) mice with the cell markers glutamine synthetase (M¨uller 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 NFjB signaling) null mouse retinas and M{\"u}uller 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.RESULTS. SP-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 M{\"u}uller 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.CONCLUSIONS. Retinal and M{\"u}ller cell SP-A is up-regulated via the NFjB pathway and upregulated 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.",

author = "Faizah Bhatti and Genevieve Ball and Ronald Hobbs and Annette Linens and Saad Munzar and Rizwan Akram and Barber, {Alistair J.} and Michael Anderson and Michael Elliott and Madeline Edwards",

note = "Publisher Copyright: {\textcopyright} 2015 The Association for Research in Vision and Ophthalmology, Inc.",

year = "2015",

month = nov,

day = "18",

doi = "10.1167/iovs.13-13652",

language = "English (US)",

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pages = "232--242",

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Bhatti, F, Ball, G, Hobbs, R, Linens, A, Munzar, S, Akram, R, Barber, AJ, Anderson, M, Elliott, M & Edwards, M 2015, 'Pulmonary surfactant protein a is expressed in mouse retina by müuller cells and impacts neovascularization in oxygen-induced retinopathy', Investigative Ophthalmology and Visual Science, vol. 56, no. 1, pp. 232-242. https://doi.org/10.1167/iovs.13-13652

TY - JOUR

T1 - Pulmonary surfactant protein a is expressed in mouse retina by müuller cells and impacts neovascularization in oxygen-induced retinopathy

AU - Bhatti, Faizah

AU - Ball, Genevieve

AU - Hobbs, Ronald

AU - Linens, Annette

AU - Munzar, Saad

AU - Akram, Rizwan

AU - Barber, Alistair J.

AU - Anderson, Michael

AU - Elliott, Michael

AU - Edwards, Madeline

PY - 2015/11/18

Y1 - 2015/11/18

N2 - PURPOSE. Surfactant 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.METHODS. Retinal SP-A was localized in wild-type (WT) mice with the cell markers glutamine synthetase (M¨uller 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 NFjB signaling) null mouse retinas and Müuller 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.RESULTS. SP-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 Müuller 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.CONCLUSIONS. Retinal and Müller cell SP-A is up-regulated via the NFjB pathway and upregulated 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.

AB - PURPOSE. Surfactant 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.METHODS. Retinal SP-A was localized in wild-type (WT) mice with the cell markers glutamine synthetase (M¨uller 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 NFjB signaling) null mouse retinas and Müuller 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.RESULTS. SP-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 Müuller 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.CONCLUSIONS. Retinal and Müller cell SP-A is up-regulated via the NFjB pathway and upregulated 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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SN - 0146-0404

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Pulmonary surfactant protein a is expressed in mouse retina by müuller cells and impacts neovascularization in oxygen-induced retinopathy

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