Abstract | BACKGROUND: METHODS: C57BL/6 J pups were placed in a 75% oxygen environment on postnatal day 7 (P7) for 5 days and then returned to room air. The co-localization of TNF-alpha with macrophages/microglia in the ischemic retina was examined by fluorescent immunohistochemistry. Bovine retinal glial cells were isolated for Northern blot analysis to quantify the expression levels of monocyte chemotactic protein-1 (MCP-1), IL-8, bFGF, and VEGF. RESULTS: Double staining of retinas revealed that the TNF-alpha expression level was enhanced in macrophages/microglia 4 days after the hypoxia. Cellular mRNA levels of MCP-1, IL-8, and bFGF, but not VEGF, were increased after treating retinal glial cells with TNF-alpha (100 U/ml). CONCLUSIONS: The results indicate that TNF-alpha is produced by activated macrophages/microglia and may participate in retinal neovascularization during post-ischemic inflammation through the induction of potent angiogenic factors in an autocrine or paracrine manner.
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Authors | Shigeo Yoshida, Ayako Yoshida, Tatsuro Ishibashi |
Journal | Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie
(Graefes Arch Clin Exp Ophthalmol)
Vol. 242
Issue 5
Pg. 409-13
(May 2004)
ISSN: 0721-832X [Print] Germany |
PMID | 15029502
(Publication Type: Journal Article)
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Chemical References |
- Chemokine CCL2
- Interleukin-8
- RNA, Messenger
- Tumor Necrosis Factor-alpha
- Fibroblast Growth Factor 2
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Topics |
- Animals
- Blotting, Northern
- Chemokine CCL2
(biosynthesis, genetics)
- Fibroblast Growth Factor 2
(biosynthesis, genetics)
- Fluorescent Antibody Technique, Indirect
- Interleukin-8
(biosynthesis, genetics)
- Macrophage Activation
- Mice
- Mice, Inbred C57BL
- Microglia
(drug effects, metabolism)
- Polymerase Chain Reaction
- RNA, Messenger
(metabolism)
- Reperfusion Injury
(metabolism)
- Retina
(drug effects, metabolism)
- Retinal Neovascularization
(metabolism)
- Tumor Necrosis Factor-alpha
(metabolism, pharmacology)
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