| pubmed-article:18602389 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18602389 | lifeskim:mentions | umls-concept:C0206745 | lld:lifeskim |
| pubmed-article:18602389 | lifeskim:mentions | umls-concept:C0027686 | lld:lifeskim |
| pubmed-article:18602389 | lifeskim:mentions | umls-concept:C0022568 | lld:lifeskim |
| pubmed-article:18602389 | lifeskim:mentions | umls-concept:C0005446 | lld:lifeskim |
| pubmed-article:18602389 | lifeskim:mentions | umls-concept:C1444749 | lld:lifeskim |
| pubmed-article:18602389 | lifeskim:mentions | umls-concept:C1415620 | lld:lifeskim |
| pubmed-article:18602389 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:18602389 | pubmed:dateCreated | 2008-9-9 | lld:pubmed |
| pubmed-article:18602389 | pubmed:abstractText | Heme oxygenase (HO-1 and HO-2) represents an intrinsic cytoprotective and anti-inflammatory system based on its ability to modulate leukocyte migration and to inhibit expression of inflammatory cytokines and proteins. HO-2 deletion leads to unresolved corneal inflammation and chronic inflammatory complications including ulceration, perforation and neovascularization. We examined the consequences of HO-2 deletion on hemangiogenesis and lymphangiogenesis in the model of suture-induced inflammatory neovascularization. An 8.0 silk suture was placed at the corneal apex of wild type and HO-2 null mice. Neovascularization was assessed by vital microscopy and quantified by image analysis. Hemangiogenesis and lymphangiogenesis were determined by immunofluorescence staining using anti-CD31 and anti-LYVE-1 antibodies, respectively. Inflammation was quantified by histology and myeloperoxidase activity. The levels of HO-1 expression and inflammatory cytokines were determined by real time PCR and ELISA, respectively. Corneal sutures produced a consistent inflammatory response and a time-dependent neovascularization. The response in HO-2 null mice was associated with a greater increase compared to the wild type in the number of leukocytes (827,600+/-129,000 vs. 294,500+/-57,510; p<0.05), neovessels measured by vital microscopy (21.91+/-1.05 vs. 12.77+/-1.55 mm; p<0.001) 4 days after suture placement. Hemangiogenesis but not lymphangiogenesis was more pronounced in HO-2 null mice compared to wild type mice. Induction of HO-1 in sutured corneas was greatly attenuated in HO-2 null corneas and treatment with biliverdin diminished the exaggerated inflammatory and neovascular response in HO-2 null mice. The demonstration that the inflammatory responses, including expression of proinflammatory proteins, inflammatory cell influx and hemangiogenesis are exaggerated in HO-2 knockout mice strongly supports the notion that the HO system is critical for controlling the inflammatory and neovascular response in the cornea. Hence, pharmacological amplification of this system may constitute a novel therapeutic strategy for the treatment of corneal disorders associated with excessive inflammation and neovascularization. | lld:pubmed |
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| pubmed-article:18602389 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18602389 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18602389 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:18602389 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:18602389 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18602389 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:18602389 | pubmed:issn | 1096-0007 | lld:pubmed |
| pubmed-article:18602389 | pubmed:author | pubmed-author:Laniado-Schwa... | lld:pubmed |
| pubmed-article:18602389 | pubmed:author | pubmed-author:DunnMichael... | lld:pubmed |
| pubmed-article:18602389 | pubmed:author | pubmed-author:BellnerLarsL | lld:pubmed |
| pubmed-article:18602389 | pubmed:author | pubmed-author:PatilKiran... | lld:pubmed |
| pubmed-article:18602389 | pubmed:author | pubmed-author:VittoMarcoM | lld:pubmed |
| pubmed-article:18602389 | pubmed:author | pubmed-author:ReganRaymondR | lld:pubmed |
| pubmed-article:18602389 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18602389 | pubmed:volume | 87 | lld:pubmed |
| pubmed-article:18602389 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18602389 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18602389 | pubmed:pagination | 268-78 | lld:pubmed |
| pubmed-article:18602389 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:18602389 | pubmed:meshHeading | pubmed-meshheading:18602389... | lld:pubmed |
