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Loss of Smooth Muscle α-Actin Leads to NF-κB-Dependent Increased Sensitivity to Angiotensin II in Smooth Muscle Cells and Aortic Enlargement.
Chen, Jiyuan; Peters, Andrew; Papke, Christina L; Villamizar, Carlos; Ringuette, Lea-Jeanne; Cao, Jiumei; Wang, Shanzhi; Ma, Shuangtao; Gong, Limin; Byanova, Katerina L; Xiong, Jian; Zhu, Michael X; Madonna, Rosalinda; Kee, Patrick; Geng, Yong-Jian; Brasier, Allan R; Davis, Elaine C; Prakash, Siddharth; Kwartler, Callie S; Milewicz, Dianna M.
Afiliación
  • Chen J; From the Departments of Internal Medicine (J.C., A.P., C.L.P., C.V., J.C., S.W., S.M., L.G., K.L.B., R.M., P.K., Y.-J.G., S.P., C.S.K., D.M.M.) and Integrative Biology and Pharmacology (J.X., M.X.Z.), The University of Texas Health Science Center at Houston; Anatomy and Cell Biology, Strathcona Anat
  • Peters A; From the Departments of Internal Medicine (J.C., A.P., C.L.P., C.V., J.C., S.W., S.M., L.G., K.L.B., R.M., P.K., Y.-J.G., S.P., C.S.K., D.M.M.) and Integrative Biology and Pharmacology (J.X., M.X.Z.), The University of Texas Health Science Center at Houston; Anatomy and Cell Biology, Strathcona Anat
  • Papke CL; From the Departments of Internal Medicine (J.C., A.P., C.L.P., C.V., J.C., S.W., S.M., L.G., K.L.B., R.M., P.K., Y.-J.G., S.P., C.S.K., D.M.M.) and Integrative Biology and Pharmacology (J.X., M.X.Z.), The University of Texas Health Science Center at Houston; Anatomy and Cell Biology, Strathcona Anat
  • Villamizar C; From the Departments of Internal Medicine (J.C., A.P., C.L.P., C.V., J.C., S.W., S.M., L.G., K.L.B., R.M., P.K., Y.-J.G., S.P., C.S.K., D.M.M.) and Integrative Biology and Pharmacology (J.X., M.X.Z.), The University of Texas Health Science Center at Houston; Anatomy and Cell Biology, Strathcona Anat
  • Ringuette LJ; From the Departments of Internal Medicine (J.C., A.P., C.L.P., C.V., J.C., S.W., S.M., L.G., K.L.B., R.M., P.K., Y.-J.G., S.P., C.S.K., D.M.M.) and Integrative Biology and Pharmacology (J.X., M.X.Z.), The University of Texas Health Science Center at Houston; Anatomy and Cell Biology, Strathcona Anat
  • Cao J; From the Departments of Internal Medicine (J.C., A.P., C.L.P., C.V., J.C., S.W., S.M., L.G., K.L.B., R.M., P.K., Y.-J.G., S.P., C.S.K., D.M.M.) and Integrative Biology and Pharmacology (J.X., M.X.Z.), The University of Texas Health Science Center at Houston; Anatomy and Cell Biology, Strathcona Anat
  • Wang S; From the Departments of Internal Medicine (J.C., A.P., C.L.P., C.V., J.C., S.W., S.M., L.G., K.L.B., R.M., P.K., Y.-J.G., S.P., C.S.K., D.M.M.) and Integrative Biology and Pharmacology (J.X., M.X.Z.), The University of Texas Health Science Center at Houston; Anatomy and Cell Biology, Strathcona Anat
  • Ma S; From the Departments of Internal Medicine (J.C., A.P., C.L.P., C.V., J.C., S.W., S.M., L.G., K.L.B., R.M., P.K., Y.-J.G., S.P., C.S.K., D.M.M.) and Integrative Biology and Pharmacology (J.X., M.X.Z.), The University of Texas Health Science Center at Houston; Anatomy and Cell Biology, Strathcona Anat
  • Gong L; From the Departments of Internal Medicine (J.C., A.P., C.L.P., C.V., J.C., S.W., S.M., L.G., K.L.B., R.M., P.K., Y.-J.G., S.P., C.S.K., D.M.M.) and Integrative Biology and Pharmacology (J.X., M.X.Z.), The University of Texas Health Science Center at Houston; Anatomy and Cell Biology, Strathcona Anat
  • Byanova KL; From the Departments of Internal Medicine (J.C., A.P., C.L.P., C.V., J.C., S.W., S.M., L.G., K.L.B., R.M., P.K., Y.-J.G., S.P., C.S.K., D.M.M.) and Integrative Biology and Pharmacology (J.X., M.X.Z.), The University of Texas Health Science Center at Houston; Anatomy and Cell Biology, Strathcona Anat
  • Xiong J; From the Departments of Internal Medicine (J.C., A.P., C.L.P., C.V., J.C., S.W., S.M., L.G., K.L.B., R.M., P.K., Y.-J.G., S.P., C.S.K., D.M.M.) and Integrative Biology and Pharmacology (J.X., M.X.Z.), The University of Texas Health Science Center at Houston; Anatomy and Cell Biology, Strathcona Anat
  • Zhu MX; From the Departments of Internal Medicine (J.C., A.P., C.L.P., C.V., J.C., S.W., S.M., L.G., K.L.B., R.M., P.K., Y.-J.G., S.P., C.S.K., D.M.M.) and Integrative Biology and Pharmacology (J.X., M.X.Z.), The University of Texas Health Science Center at Houston; Anatomy and Cell Biology, Strathcona Anat
  • Madonna R; From the Departments of Internal Medicine (J.C., A.P., C.L.P., C.V., J.C., S.W., S.M., L.G., K.L.B., R.M., P.K., Y.-J.G., S.P., C.S.K., D.M.M.) and Integrative Biology and Pharmacology (J.X., M.X.Z.), The University of Texas Health Science Center at Houston; Anatomy and Cell Biology, Strathcona Anat
  • Kee P; From the Departments of Internal Medicine (J.C., A.P., C.L.P., C.V., J.C., S.W., S.M., L.G., K.L.B., R.M., P.K., Y.-J.G., S.P., C.S.K., D.M.M.) and Integrative Biology and Pharmacology (J.X., M.X.Z.), The University of Texas Health Science Center at Houston; Anatomy and Cell Biology, Strathcona Anat
  • Geng YJ; From the Departments of Internal Medicine (J.C., A.P., C.L.P., C.V., J.C., S.W., S.M., L.G., K.L.B., R.M., P.K., Y.-J.G., S.P., C.S.K., D.M.M.) and Integrative Biology and Pharmacology (J.X., M.X.Z.), The University of Texas Health Science Center at Houston; Anatomy and Cell Biology, Strathcona Anat
  • Brasier AR; From the Departments of Internal Medicine (J.C., A.P., C.L.P., C.V., J.C., S.W., S.M., L.G., K.L.B., R.M., P.K., Y.-J.G., S.P., C.S.K., D.M.M.) and Integrative Biology and Pharmacology (J.X., M.X.Z.), The University of Texas Health Science Center at Houston; Anatomy and Cell Biology, Strathcona Anat
  • Davis EC; From the Departments of Internal Medicine (J.C., A.P., C.L.P., C.V., J.C., S.W., S.M., L.G., K.L.B., R.M., P.K., Y.-J.G., S.P., C.S.K., D.M.M.) and Integrative Biology and Pharmacology (J.X., M.X.Z.), The University of Texas Health Science Center at Houston; Anatomy and Cell Biology, Strathcona Anat
  • Prakash S; From the Departments of Internal Medicine (J.C., A.P., C.L.P., C.V., J.C., S.W., S.M., L.G., K.L.B., R.M., P.K., Y.-J.G., S.P., C.S.K., D.M.M.) and Integrative Biology and Pharmacology (J.X., M.X.Z.), The University of Texas Health Science Center at Houston; Anatomy and Cell Biology, Strathcona Anat
  • Kwartler CS; From the Departments of Internal Medicine (J.C., A.P., C.L.P., C.V., J.C., S.W., S.M., L.G., K.L.B., R.M., P.K., Y.-J.G., S.P., C.S.K., D.M.M.) and Integrative Biology and Pharmacology (J.X., M.X.Z.), The University of Texas Health Science Center at Houston; Anatomy and Cell Biology, Strathcona Anat
  • Milewicz DM; From the Departments of Internal Medicine (J.C., A.P., C.L.P., C.V., J.C., S.W., S.M., L.G., K.L.B., R.M., P.K., Y.-J.G., S.P., C.S.K., D.M.M.) and Integrative Biology and Pharmacology (J.X., M.X.Z.), The University of Texas Health Science Center at Houston; Anatomy and Cell Biology, Strathcona Anat
Circ Res ; 120(12): 1903-1915, 2017 Jun 09.
Article en En | MEDLINE | ID: mdl-28461455
RATIONALE: Mutations in ACTA2, encoding the smooth muscle isoform of α-actin, cause thoracic aortic aneurysms, acute aortic dissections, and occlusive vascular diseases. OBJECTIVE: We sought to identify the mechanism by which loss of smooth muscle α-actin causes aortic disease. METHODS AND RESULTS: Acta2-/- mice have an increased number of elastic lamellae in the ascending aorta and progressive aortic root dilation as assessed by echocardiography that can be attenuated by treatment with losartan, an angiotensin II (AngII) type 1 receptor blocker. AngII levels are not increased in Acta2-/- aortas or kidneys. Aortic tissue and explanted smooth muscle cells from Acta2-/- aortas show increased production of reactive oxygen species and increased basal nuclear factor κB signaling, leading to an increase in the expression of the AngII receptor type I a and activation of signaling at 100-fold lower levels of AngII in the mutant compared with wild-type cells. Furthermore, disruption of smooth muscle α-actin filaments in wild-type smooth muscle cells by various mechanisms activates nuclear factor κB signaling and increases expression of AngII receptor type I a. CONCLUSIONS: These findings reveal that disruption of smooth muscle α-actin filaments in smooth muscle cells increases reactive oxygen species levels, activates nuclear factor κB signaling, and increases AngII receptor type I a expression, thus potentiating AngII signaling in vascular smooth muscle cells without an increase in the exogenous levels of AngII.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Aorta Torácica / Angiotensina II / FN-kappa B / Actinas / Miocitos del Músculo Liso / Receptor de Angiotensina Tipo 1 Tipo de estudio: Diagnostic_studies / Prognostic_studies Límite: Animals Idioma: En Revista: Circ Res Año: 2017 Tipo del documento: Article Pais de publicación: Estados Unidos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Aorta Torácica / Angiotensina II / FN-kappa B / Actinas / Miocitos del Músculo Liso / Receptor de Angiotensina Tipo 1 Tipo de estudio: Diagnostic_studies / Prognostic_studies Límite: Animals Idioma: En Revista: Circ Res Año: 2017 Tipo del documento: Article Pais de publicación: Estados Unidos