Increased expression of chemokine KC, an interleukin-8 homologue, in a model of oxygen-induced retinopathy

Michael (Mike) Powers, Michael H. Davies, Joshua P. Eubanks

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Purpose: The purpose of this study was to determine the retinal expression of angiogenic chemokines/cytokines in a mouse model of oxygen-induced retinopathy. Methods: C57BL/6 (B6) mice were exposed to 75% oxygen from postnatal day 7 (P7) to P12 and then recovered in room air. Reverse transcription-polymerase chain reaction (RT-PCR) was used to determine relative mRNA levels of KC, macrophage inflammatory protein-2 (MIP-2), interleukin-1a (IL-1α), and interferon gamma (IFN-γ). Immunohistochemistry was used to localize KC in the retina. IL-1α was also injected into the vitreous of mouse eyes, and KC expression was examined by RT-PCR, enzyme-linked immunosorbent assay (ELISA), and immunohistochemistry. Results: KC expression at both the mRNA and protein levels was increased in P14, P17, and P21 of hyperoxia-injured eyes. KC immunoreactivity was localized along the nerve fiber layer and in radial Müller cell processes. IL-1α mRNA was modestly increased in hyperoxia-injured eyes on P14 and P17. INF-γ mRNA was not detected in the retina. Adult mouse eyes injected with IL-1α demonstrated increased levels of both KC mRNA and protein, with KC immunoreactivity localized to Müller cell processes. Conclusions: Oxygen-induced injury to the developing retina results in the induction of the CXC chemokine KC at both the mRNA and protein levels during the peak time points of neovascularization, suggesting a possible role in the pathogenesis of retinopathy of prematurity. Copyriqht

Original languageEnglish (US)
Pages (from-to)299-307
Number of pages9
JournalCurrent Eye Research
Volume30
Issue number4
DOIs
StatePublished - Apr 2005

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Interleukin-8
Chemokines
Interleukins
Oxygen
Messenger RNA
Retina
Hyperoxia
Reverse Transcription
Immunohistochemistry
Chemokine CXCL2
CXC Chemokines
Polymerase Chain Reaction
Retinopathy of Prematurity
Proteins
Nerve Fibers
Interferon-gamma
Enzyme-Linked Immunosorbent Assay
Air
Cytokines
Wounds and Injuries

Keywords

  • Angiogenesis
  • Chemokines
  • IL-8
  • Neovascularization
  • ROP

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems

Cite this

Increased expression of chemokine KC, an interleukin-8 homologue, in a model of oxygen-induced retinopathy. / Powers, Michael (Mike); Davies, Michael H.; Eubanks, Joshua P.

In: Current Eye Research, Vol. 30, No. 4, 04.2005, p. 299-307.

Research output: Contribution to journalArticle

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abstract = "Purpose: The purpose of this study was to determine the retinal expression of angiogenic chemokines/cytokines in a mouse model of oxygen-induced retinopathy. Methods: C57BL/6 (B6) mice were exposed to 75{\%} oxygen from postnatal day 7 (P7) to P12 and then recovered in room air. Reverse transcription-polymerase chain reaction (RT-PCR) was used to determine relative mRNA levels of KC, macrophage inflammatory protein-2 (MIP-2), interleukin-1a (IL-1α), and interferon gamma (IFN-γ). Immunohistochemistry was used to localize KC in the retina. IL-1α was also injected into the vitreous of mouse eyes, and KC expression was examined by RT-PCR, enzyme-linked immunosorbent assay (ELISA), and immunohistochemistry. Results: KC expression at both the mRNA and protein levels was increased in P14, P17, and P21 of hyperoxia-injured eyes. KC immunoreactivity was localized along the nerve fiber layer and in radial M{\"u}ller cell processes. IL-1α mRNA was modestly increased in hyperoxia-injured eyes on P14 and P17. INF-γ mRNA was not detected in the retina. Adult mouse eyes injected with IL-1α demonstrated increased levels of both KC mRNA and protein, with KC immunoreactivity localized to M{\"u}ller cell processes. Conclusions: Oxygen-induced injury to the developing retina results in the induction of the CXC chemokine KC at both the mRNA and protein levels during the peak time points of neovascularization, suggesting a possible role in the pathogenesis of retinopathy of prematurity. Copyriqht",
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N2 - Purpose: The purpose of this study was to determine the retinal expression of angiogenic chemokines/cytokines in a mouse model of oxygen-induced retinopathy. Methods: C57BL/6 (B6) mice were exposed to 75% oxygen from postnatal day 7 (P7) to P12 and then recovered in room air. Reverse transcription-polymerase chain reaction (RT-PCR) was used to determine relative mRNA levels of KC, macrophage inflammatory protein-2 (MIP-2), interleukin-1a (IL-1α), and interferon gamma (IFN-γ). Immunohistochemistry was used to localize KC in the retina. IL-1α was also injected into the vitreous of mouse eyes, and KC expression was examined by RT-PCR, enzyme-linked immunosorbent assay (ELISA), and immunohistochemistry. Results: KC expression at both the mRNA and protein levels was increased in P14, P17, and P21 of hyperoxia-injured eyes. KC immunoreactivity was localized along the nerve fiber layer and in radial Müller cell processes. IL-1α mRNA was modestly increased in hyperoxia-injured eyes on P14 and P17. INF-γ mRNA was not detected in the retina. Adult mouse eyes injected with IL-1α demonstrated increased levels of both KC mRNA and protein, with KC immunoreactivity localized to Müller cell processes. Conclusions: Oxygen-induced injury to the developing retina results in the induction of the CXC chemokine KC at both the mRNA and protein levels during the peak time points of neovascularization, suggesting a possible role in the pathogenesis of retinopathy of prematurity. Copyriqht

AB - Purpose: The purpose of this study was to determine the retinal expression of angiogenic chemokines/cytokines in a mouse model of oxygen-induced retinopathy. Methods: C57BL/6 (B6) mice were exposed to 75% oxygen from postnatal day 7 (P7) to P12 and then recovered in room air. Reverse transcription-polymerase chain reaction (RT-PCR) was used to determine relative mRNA levels of KC, macrophage inflammatory protein-2 (MIP-2), interleukin-1a (IL-1α), and interferon gamma (IFN-γ). Immunohistochemistry was used to localize KC in the retina. IL-1α was also injected into the vitreous of mouse eyes, and KC expression was examined by RT-PCR, enzyme-linked immunosorbent assay (ELISA), and immunohistochemistry. Results: KC expression at both the mRNA and protein levels was increased in P14, P17, and P21 of hyperoxia-injured eyes. KC immunoreactivity was localized along the nerve fiber layer and in radial Müller cell processes. IL-1α mRNA was modestly increased in hyperoxia-injured eyes on P14 and P17. INF-γ mRNA was not detected in the retina. Adult mouse eyes injected with IL-1α demonstrated increased levels of both KC mRNA and protein, with KC immunoreactivity localized to Müller cell processes. Conclusions: Oxygen-induced injury to the developing retina results in the induction of the CXC chemokine KC at both the mRNA and protein levels during the peak time points of neovascularization, suggesting a possible role in the pathogenesis of retinopathy of prematurity. Copyriqht

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