Current eye research · 2005
Increased expression of chemokine KC, an interleukin-8 homologue, in a model of oxygen-induced retinopathy.
СтатьяПоддержка NIH: внешняя программаПоддержка службы здравоохранения СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Powers Michael R, Davies Michael H, Eubanks Joshua P
Аннотация
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-1alpha (IL-1alpha), and interferon gamma (IFN-gamma). Immunohistochemistry was used to localize KC in the retina. IL-1alpha 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-1alpha mRNA was modestly increased in hyperoxia-injured eyes on P14 and P17. INF-gamma mRNA was not detected in the retina. Adult mouse eyes injected with IL-1alpha 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.
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-1alpha (IL-1alpha), and interferon gamma (IFN-gamma). Immunohistochemistry was used to localize KC in the retina. IL-1alpha 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-1alpha mRNA was modestly increased in hyperoxia-injured eyes on P14 and P17. INF-gamma mRNA was not detected in the retina. Adult mouse eyes injected with IL-1alpha 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.
Предметные рубрики MeSH
AnimalsAnimals, NewbornChemokine CXCL1Chemokine CXCL2ChemokinesChemokines, CXCDisease Models, AnimalEnzyme-Linked Immunosorbent AssayGene ExpressionHyperoxiaImmunohistochemistryIntercellular Signaling Peptides and ProteinsInterferon-gammaInterleukin-1Interleukin-8MiceMice, Inbred C57BLOxygenRNA, MessengerRetinal NeovascularizationReverse Transcriptase Polymerase Chain Reaction