Statin-induced expression of CD59 on vascular endothelium in hypoxia a potential mechanism for the anti-inflammatory actions of statins in rheumatoid arthritis 英文参考文献.docVIP

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Statin-induced expression of CD59 on vascular endothelium in hypoxia a potential mechanism for the anti-inflammatory actions of statins in rheumatoid arthritis 英文参考文献.doc

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Statin-induced expression of CD59 on vascular endothelium in hypoxia a potential mechanism for the anti-inflammatory actions of statins in rheumatoid arthritis 英文参考文献

Available online /content/8/4/R130 Research article Open Access Vol 8 No 4 Statin-induced expression of CD59 on vascular endothelium in hypoxia: a potential mechanism for the anti-inflammatory actions of statins in rheumatoid arthritis Anne R Kinderlerer1, Rivka Steinberg1, Michael Johns1, Sarah K Harten2, Elaine A Lidington1, Dorian O Haskard1, Patrick H Maxwell2 and Justin C Mason1 1Cardiovascular Medicine Unit, Eric Bywaters Center for Vascular Inflammation, Imperial College London, Hammersmith Hospital, London, UK 2The Renal Unit, Imperial College London, Hammersmith Hospital, London, UK Corresponding author: Justin C Mason, justin.mason@imperial.ac.uk Received: 30 Jan 2006 Revisions requested: 21 Mar 2006 Revisions received: 3 Jul 2006 Accepted: 21 Jul 2006 Published: 21 Jul 2006 Arthritis Research Therapy 2006, 8:R130 (doi:10.1186/ar2019) This article is online at: /content/8/4/R130 ? 2006 Kinderlerer et al., licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Hypoxia, which leads to dysfunctional cell metabolism, and activation both play central roles in the protein expression in hypoxia was associated with an increase in steady-state mRNA. L-Mevalonate and geranylgeraniol reversed the response, confirming a role for inhibition of 3-hydroxy-3- methylglutaryl coenzyme A reductase and geranylgeranylation. Likewise, inhibition by NG-monomethyl-L-arginine and NG-nitro- L-arginine methyl ester confirmed that CD59 upregulation in hypoxia was nitric oxide dependent. The expression of another complement-inhibitory protein, decay-accelerating factor (DAF), is known to be increased by atorvastatin in normoxia; this response was also significantly enhanced under hypoxic