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 Barber, Michael Anderson, Michael Elliott, Madeline Edwards

Research output: Contribution to journalArticle

8 Citations (Scopus)

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 languageEnglish (US)
Pages (from-to)232-242
Number of pages11
JournalInvestigative Ophthalmology and Visual Science
Volume56
Issue number1
DOIs
StatePublished - Nov 18 2015

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Pulmonary Surfactant-Associated Proteins
Pulmonary Surfactant-Associated Protein A
Ependymoglial Cells
Retina
Oxygen
Glutamate-Ammonia Ligase
Up-Regulation
Myeloid Differentiation Factor 88
Retinal Neovascularization
Retinaldehyde
Ligands
Toll-Like Receptor 2
Toll-Like Receptor 4

All Science Journal Classification (ASJC) codes

  • Ophthalmology
  • Sensory Systems
  • Cellular and Molecular Neuroscience

Cite this

Bhatti, Faizah ; Ball, Genevieve ; Hobbs, Ronald ; Linens, Annette ; Munzar, Saad ; Akram, Rizwan ; Barber, Alistair ; Anderson, Michael ; Elliott, Michael ; Edwards, Madeline. / Pulmonary surfactant protein a is expressed in mouse retina by müuller cells and impacts neovascularization in oxygen-induced retinopathy. In: Investigative Ophthalmology and Visual Science. 2015 ; Vol. 56, No. 1. pp. 232-242.
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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 Alistair Barber and Michael Anderson and Michael Elliott and Madeline Edwards",
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Pulmonary surfactant protein a is expressed in mouse retina by müuller cells and impacts neovascularization in oxygen-induced retinopathy. / Bhatti, Faizah; Ball, Genevieve; Hobbs, Ronald; Linens, Annette; Munzar, Saad; Akram, Rizwan; Barber, Alistair; Anderson, Michael; Elliott, Michael; Edwards, Madeline.

In: Investigative Ophthalmology and Visual Science, Vol. 56, No. 1, 18.11.2015, p. 232-242.

Research output: Contribution to journalArticle

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

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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