Mechanisms of Vascular Smooth Muscle NADPH Oxidase 1 (Nox1) Contribution to Injury-Induced Neointimal Formation
| العنوان: | Mechanisms of Vascular Smooth Muscle NADPH Oxidase 1 (Nox1) Contribution to Injury-Induced Neointimal Formation |
|---|---|
| المؤلفون: | Botond Banfi, Alejandra San Martin, S. Raju Datla, Bernard Lassègue, Anna Dikalova, Erin Lyons, Abel Martin Garrido, Karl-Heinz Krause, Puja K. Mehta, Moo Yeol Lee, Kathy K. Griendling, J. David Lambeth |
| المصدر: | Arteriosclerosis, Thrombosis, and Vascular Biology, Vol. 29, No 4 (2009) pp. 480-487 |
| بيانات النشر: | Ovid Technologies (Wolters Kluwer Health), 2009. |
| سنة النشر: | 2009 |
| مصطلحات موضوعية: | Time Factors, Vascular smooth muscle, Apoptosis, Carrier Proteins/metabolism, ddc:616.07, 030204 cardiovascular system & hematology, Muscle, Smooth, Vascular, Extracellular matrix, Mice, 0302 clinical medicine, Cell Movement, NADH, NADPH Oxidoreductases, Phosphorylation, Cells, Cultured, Mice, Knockout, 0303 health sciences, NADPH Oxidase 1, Cofilin, Cell biology, Femoral Artery, Biochemistry, NOX1, cardiovascular system, Fibronectins/metabolism, Cardiology and Cardiovascular Medicine, p21-Activated Kinases/metabolism, Neointima, Cofilin 2, Formins, Collagen Type I/metabolism, Biology, Transfection, Collagen Type I, Article, 03 medical and health sciences, Animals, Genetically modified animal, Cell Proliferation, 030304 developmental biology, Hyperplasia, Femoral Artery/enzymology/injuries, NADH, NADPH Oxidoreductases/deficiency/genetics/ metabolism, Muscle, Smooth, Vascular/ enzymology/injuries/pathology, Fibronectins, Mice, Inbred C57BL, Fibronectin, Disease Models, Animal, p21-Activated Kinases, Tunica Intima/ enzymology/injuries/pathology, Cofilin 2/metabolism, biology.protein, Carrier Proteins, Tunica Intima |
| الوصف: | Objective— Vascular NADPH oxidases (Noxes) have been implicated in cardiovascular diseases; however, the importance of individual Nox homologues remains unclear. Here, the role of the vascular smooth muscle cell (VSMC) Nox1 in neointima formation was studied using genetically modified animal models. Methods and Results— Wire injury–induced neointima formation in the femoral artery, along with proliferation and apoptosis, was reduced in Nox1 y/− mice, but there was little difference in Tg SMCnox1 mice compared with wild-type (WT) mice. Proliferation and migration were reduced in cultured Nox1 y/− VSMCs and increased in Tg SMCnox1 cells. Tg SMCnox1 cells exhibited increased fibronectin secretion, but neither collagen I production nor cell adhesion was affected by alteration of Nox1. Using antibody microarray and Western blotting analysis, increased cofilin phosphorylation and mDia1 expression and decreased PAK1 expression were detected in Nox1 y/− cells. Overexpression of S3A, a constitutively active cofilin mutant, partially recovered reduced migration of Nox1 y/− cells, suggesting that reduction in cofilin activity contributes to impaired migration of Nox1 y/− VSMCs. Conclusions— These results indicate that Nox1 plays a critical role in neointima formation by mediating VSMC migration, proliferation, and extracellular matrix production, and that cofilin is a major effector of Nox1-mediated migration. Inhibition of Nox1 may be an efficient strategy to suppress neointimal formation. |
| تدمد: | 1524-4636 1079-5642 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6045bd80edd366d250fd48b6d1061778Test https://doi.org/10.1161/atvbaha.108.181925Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....6045bd80edd366d250fd48b6d1061778 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15244636 10795642 |
|---|