NFATc3 Mediates Chronic Hypoxia-induced Pulmonary Arterial Remodeling with α-Actin Up-regulation*
暂无分享,去创建一个
Sergio de Frutos | Rhyannon Spangler | Dominique Alò | Laura V. González Bosc | Dominique Alò | S. de Frutos | Rhyannon Spangler | L. V. Bosc
[1] Thomas D. Schmittgen,et al. Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. , 2001, Methods.
[2] Y. El-Gamal,et al. Plasma endothelin-1 immunoreactivity in asthmatic children. , 2002, Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology.
[3] X. Bigard,et al. Cyclosporin A inhibits hypoxia-induced pulmonary hypertension and right ventricle hypertrophy. , 2006, American journal of respiratory and critical care medicine.
[4] J. Orens,et al. Dysfunctional voltage-gated K+ channels in pulmonary artery smooth muscle cells of patients with primary pulmonary hypertension. , 1998, Circulation.
[5] M. Nelson,et al. NFAT regulation in smooth muscle. , 2003, Trends in cardiovascular medicine.
[6] A. Nadas,et al. Rat pulmonary circulation after chronic hypoxia: hemodynamic and structural features. , 1979, The American journal of physiology.
[7] M. Nelson,et al. NFAT4 Movement in Native Smooth Muscle , 2001, The Journal of Biological Chemistry.
[8] S. Sasayama,et al. Calcineurin-GATA-6 pathway is involved in smooth muscle–specific transcription , 2002, The Journal of cell biology.
[9] G. Owens,et al. Regulation of differentiation of vascular smooth muscle cells. , 1995, Physiological reviews.
[10] W. Seeger,et al. Activation of Soluble Guanylate Cyclase Reverses Experimental Pulmonary Hypertension and Vascular Remodeling , 2006, Circulation.
[11] L. Shimoda,et al. Altered pulmonary vasoreactivity in the chronically hypoxic lung. , 2000, Physiological research.
[12] J. Molkentin,et al. Targeted Disruption of NFATc3, but Not NFATc4, Reveals an Intrinsic Defect in Calcineurin-Mediated Cardiac Hypertrophic Growth , 2002, Molecular and Cellular Biology.
[13] G. Semenza,et al. Partial HIF-1alpha deficiency impairs pulmonary arterial myocyte electrophysiological responses to hypoxia. , 2001, American journal of physiology. Lung cellular and molecular physiology.
[14] G. Owens. Molecular control of vascular smooth muscle cell differentiation. , 1998, Acta physiologica Scandinavica.
[15] P. Rabinovitch,et al. Smooth muscle cell hypertrophy versus hyperplasia in hypertension. , 1981, Proceedings of the National Academy of Sciences of the United States of America.
[16] G. Owens,et al. Molecular regulation of vascular smooth muscle cell differentiation in development and disease. , 2004, Physiological reviews.
[17] Paul McLoughlin,et al. The structural basis of pulmonary hypertension in chronic lung disease: remodelling, rarefaction or angiogenesis? , 2002, Journal of anatomy.
[18] Y. Ohkawa,et al. Calcineurin-mediated pathway involved in the differentiated phenotype of smooth muscle cells. , 2003, Biochemical and biophysical research communications.
[19] S. Earley,et al. Pressure-induced smooth muscle cell depolarization in pulmonary arteries from control and chronically hypoxic rats does not cause myogenic vasoconstriction. , 2005, Journal of applied physiology.
[20] Lin Chen,et al. Transcriptional regulation by calcium, calcineurin, and NFAT. , 2003, Genes & development.
[21] W. Steudel,et al. alpha-smooth-muscle actin and microvascular precursor smooth-muscle cells in pulmonary hypertension. , 1999, American journal of respiratory cell and molecular biology.
[22] K. Stenmark,et al. Hypoxia induces differentiation of pulmonary artery adventitial fibroblasts into myofibroblasts. , 2004, American journal of physiology. Cell physiology.
[23] A. Fujimori,et al. A novel and selective endothelin ET(A) receptor antagonist YM598 prevents the development of chronic hypoxia-induced pulmonary hypertension in rats. , 2005, Vascular pharmacology.
[24] W. Kummer,et al. Rapamycin attenuates hypoxia-induced pulmonary vascular remodeling and right ventricular hypertrophy in mice , 2007, Respiratory research.
[25] G. Crabtree,et al. Cyclosporin A specifically inhibits function of nuclear proteins involved in T cell activation. , 1989, Science.
[26] E. Silverman,et al. Primary pulmonary hypertension in a patient with systemic-onset juvenile arthritis. , 2010, Arthritis and rheumatism.
[27] I. Fantozzi,et al. Enhanced expression of transient receptor potential channels in idiopathic pulmonary arterial hypertension. , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[28] K. Morris,et al. Involvement of RhoA/Rho kinase signaling in pulmonary hypertension of the fawn-hooded rat. , 2006, Journal of applied physiology.
[29] K. Stenmark,et al. Mechanisms of structural remodeling in chronic pulmonary hypertension. , 1999, Pediatrics in review.
[30] B. Walker,et al. Selective upregulation of arterial endothelial nitric oxide synthase in pulmonary hypertension. , 1997, The American journal of physiology.
[31] L. Reid,et al. Ultrastructural features of the distended pulmonary arteries of the normal rat , 1979, The Anatomical record.
[32] Mark T. Nelson,et al. Intraluminal Pressure Is a Stimulus for NFATc3 Nuclear Accumulation , 2004, Journal of Biological Chemistry.
[33] S. M. Sims,et al. Constrictor-induced translocation of NFAT3 in human and rat pulmonary artery smooth muscle. , 2005, American journal of physiology. Lung cellular and molecular physiology.
[34] K. Kaibuchi,et al. Long-Term Treatment With a Rho-Kinase Inhibitor Improves Monocrotaline-Induced Fatal Pulmonary Hypertension in Rats , 2004, Circulation research.
[35] H. Nakayama,et al. Calcineurin‐dependent cardiomyopathy is activated by TRPC in the adult mouse heart , 2006, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[36] T. Murphy,et al. Evidence that Galpha(q)-coupled receptor-induced interleukin-6 mRNA in vascular smooth muscle cells involves the nuclear factor of activated T cells. , 2000, Molecular pharmacology.
[37] L. Poellinger,et al. Signal transduction in hypoxic cells: inducible nuclear translocation and recruitment of theCBP/p300 coactivator by the hypoxia‐induciblefactor‐1α , 1998, The EMBO journal.
[38] M. Arzt,et al. Effects of ET-A receptor blockade on eNOS gene expression in chronic hypoxic rat lungs. , 2003, Journal of applied physiology.
[39] G. Semenza,et al. Hypoxia Inducible Factor 1 Mediates Hypoxia-Induced TRPC Expression and Elevated Intracellular Ca2+ in Pulmonary Arterial Smooth Muscle Cells , 2006, Circulation research.
[40] M. Nelson,et al. Constitutively Elevated Nuclear Export Activity Opposes Ca2+-dependent NFATc3 Nuclear Accumulation in Vascular Smooth Muscle , 2003, Journal of Biological Chemistry.
[41] J. Molkentin,et al. Novel blocker of NFAT activation inhibits IL-6 production in human myometrial arteries and reduces vascular smooth muscle cell proliferation. , 2007, American journal of physiology. Cell physiology.
[42] Feng Chen,et al. Signals Transduced by Ca2+/Calcineurin and NFATc3/c4 Pattern the Developing Vasculature , 2001, Cell.
[43] P. Leung,et al. Effects of Chronic Hypoxia on the Circulating and Pancreatic Renin-Angiotensin System , 2002, Pancreas.
[44] C. Tse,et al. Chronic Hypoxia–Induced Upregulation of Store-Operated and Receptor-Operated Ca2 Channels in Pulmonary Arterial Smooth Muscle Cells: A Novel Mechanism of Hypoxic Pulmonary Hypertension , 2004, Circulation research.
[45] L. Chicoine,et al. Maintained upregulation of pulmonary eNOS gene and protein expression during recovery from chronic hypoxia. , 1999, American journal of physiology. Heart and circulatory physiology.
[46] R. Priori,et al. Pulmonary Arterial Hypertension Responsive to Immunosuppressive Therapy in Systemic Lupus Erythematosus , 1993, Lupus.
[47] B. Walker,et al. Segmental vasodilatory effectiveness of inhaled NO in lungs from chronically hypoxic rats. , 1998, Respiration physiology.
[48] S. Archer,et al. The mechanism of acute hypoxic pulmonary vasoconstriction: the tale of two channels , 1995, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[49] I. Graef,et al. NFAT signaling in vertebrate development. , 2001, Current opinion in genetics & development.
[50] M. Juhaszova,et al. Hypoxia inhibits gene expression of voltage-gated K+ channel alpha subunits in pulmonary artery smooth muscle cells. , 1997, The Journal of clinical investigation.
[51] M. Yacoub,et al. Expression of pulmonary vascular angiotensin‐converting enzyme in primary and secondary plexiform pulmonary hypertension , 2000, The Journal of pathology.
[52] M. Nishida,et al. Roles of Endothelin ETA and ETB Receptors in the Pathogenesis of Monocrotaline-Induced Pulmonary Hypertension , 2004, Journal of cardiovascular pharmacology.
[53] L. Hansson. The optimal blood pressure reduction , 1996, Journal of hypertension. Supplement : official journal of the International Society of Hypertension.
[54] A. Bonev,et al. Opposing Actions of Inositol 1,4,5-Trisphosphate and Ryanodine Receptors on Nuclear Factor of Activated T-cells Regulation in Smooth Muscle* , 2002, The Journal of Biological Chemistry.
[55] J. Molkentin,et al. Activation of NFATc3 Down-regulates the β1 Subunit of Large Conductance, Calcium-activated K+ Channels in Arterial Smooth Muscle and Contributes to Hypertension* , 2007, Journal of Biological Chemistry.
[56] G. Semenza. Perspectives on Oxygen Sensing , 1999, Cell.
[57] R. Bassel-Duby,et al. TRPC3 channels confer cellular memory of recent neuromuscular activity. , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[58] R. A. Murphy,et al. Actin and tropomyosin variants in smooth muscles. Dependence on tissue type. , 1984, The Journal of biological chemistry.
[59] M. Nelson,et al. Nuclear Factor of Activated T Cells and Serum Response Factor Cooperatively Regulate the Activity of an α-Actin Intronic Enhancer* , 2005, Journal of Biological Chemistry.
[60] D. Rodman,et al. Enhanced ETA-receptor-mediated inhibition of Kv channels in hypoxic hypertensive rat pulmonary artery myocytes. , 1999, American journal of physiology. Heart and circulatory physiology.
[61] C. Ferri,et al. Circulating endothelin-1 concentrations in patients with chronic hypoxia. , 1995, Journal of clinical pathology.
[62] J. Dubois-Randé,et al. Modulation of angiotensin II receptor expression during development and regression of hypoxic pulmonary hypertension. , 2000, American journal of respiratory cell and molecular biology.
[63] Y. Fukuchi,et al. Localization and distribution of endothelin receptor subtypes in pulmonary vasculature of normal and hypoxia-exposed rats. , 1999, American journal of respiratory cell and molecular biology.
[64] E. Olson,et al. Angiotensin II-induced stimulation of smooth muscle alpha-actin expression by serum response factor and the homeodomain transcription factor MHox. , 1997, Circulation research.
[65] K. Morris,et al. Attenuation of acute hypoxic pulmonary vasoconstriction and hypoxic pulmonary hypertension in mice by inhibition of Rho-kinase. , 2004, American journal of physiology. Lung cellular and molecular physiology.
[66] N. Morrell,et al. Angiotensin converting enzyme expression is increased in small pulmonary arteries of rats with hypoxia-induced pulmonary hypertension. , 1995, The Journal of clinical investigation.
[67] L. Glimcher,et al. The transcription factor NFAT4 is involved in the generation and survival of T cells. , 1998, Immunity.
[68] Thomas J. Murphy,et al. The Cyclosporin A-sensitive Nuclear Factor of Activated T Cells (NFAT) Proteins Are Expressed in Vascular Smooth Muscle Cells , 1998, The Journal of Biological Chemistry.
[69] P. Hogan,et al. Transcription factors of the NFAT family: regulation and function. , 1997, Annual review of immunology.