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          Institute: MPI für Herz- und Lungenforschung (W. G. Kerckhoff Institut)     Collection: Publikationen des W. G. Kerckhoff-Instituts     Display Documents



ID: 474453.0, MPI für Herz- und Lungenforschung (W. G. Kerckhoff Institut) / Publikationen des W. G. Kerckhoff-Instituts
Effects of endogenous NO and of DETA NONOate in Arteriogenesis
Authors:Troidl, K.; Tribulova, S.; Cai, W. J.; Eitenmuller, I.; Wustrack, H.; Schierling, W.; Troidl, C.; Schmitz-Rixen, T.; Schaper, W.
Date of Publication (YYYY-MM-DD):2009
Title of Journal:J Cardiovasc Pharmacol
Audience:Not Specified
Abstract / Description:Previous studies showed that targeted eNOS disruption in mice with femoral artery occlusion does not impede - and transgenic eNOS over-expression does not stimulate - collateral artery growth following femoral artery occlusion, suggesting that NO from eNOS does not play a role in arteriogenesis. However, pharmacological NOS inhibition with L-NAME markedly blocks arteriogenesis, suggestive of an important role of NO. In order to solve the paradox, we studied targeted deletion of eNOS and of iNOS in mice and found that only iNOS knockout could partially inhibit arteriogenesis. However, the combination of eNOS knockout and treatment with the iNOS inhibitor L-NIL completely abolished arteriogenesis. mRNA transcription studies (RT-PCR) performed on collateral arteries of rats showed that eNOS and especially iNOS (but not nNOS) become up-regulated in shear stress-stimulated collateral vessels, which supports the hypothesis that NO is necessary for arteriogenesis but that iNOS plays an important part. This was strengthened by the observation that the NO-donor DETA NONOate strongly stimulated collateral artery growth, activated perivascular monocytes and increased proliferation markers. Shear stress-induced NO may activate the innate immune system and activate iNOS. Conclusion: arteriogenesis is completely dependent on the presence of NO, a large part of it coming from mononuclear cells.
External Publication Status:published
Document Type:Article
Communicated by:N. N.
Affiliations:MPI für physiologische und klinische Forschung
External Affiliations:*Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany; +Xiangsha School of Medicine, Dept. of Anatomy, Central South Univ. Changsha, Hunan, China; degrees Division of Vascular and Endovascular Surgery, University of Regensburg, Germany; #Division of Vascular and Endovascular Surgery, Goethe-University Frankfurt/Main, Germany, section sign Both authors contributed equally.
Identifiers:ISSN:1533-4023 (Electronic) 1533-4023 (Linking)
URL:http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=..
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