Sex hormones and vascular protection in pulmonary arterial hypertension.

Pulmonary Arterial Hypertension (PAH) is a serious disease and a major public health problem with approximately 1000 new patients diagnosed every year in the United States.1, 2 PAH is a progressive disease involving impaired pulmonary vascular structure and function and is ultimately lethal due to right ventricular failure. Recent insights into the pathogenesis of PAH have lead to more promising therapeutic approaches and improved outcomes; however, the mortality rates associated with PAH remain unacceptably high.1, 3, 4

[1]  G. Hansmann,et al.  Design and validation of an endothelial progenitor cell capture chip and its application in patients with pulmonary arterial hypertension , 2011, Journal of Molecular Medicine.

[2]  A. Mueck,et al.  2-Methoxyestradiol—Biology and mechanism of action , 2010, Steroids.

[3]  Christopher S Coffey,et al.  Predicting Survival in Pulmonary Arterial Hypertension: Insights From the Registry to Evaluate Early and Long-Term Pulmonary Arterial Hypertension Disease Management (REVEAL) , 2010, Circulation.

[4]  Horst Olschewski,et al.  Addition of inhaled treprostinil to oral therapy for pulmonary arterial hypertension: a randomized controlled clinical trial. , 2010, Journal of the American College of Cardiology.

[5]  G. Raskob,et al.  Pulmonary arterial hypertension: baseline characteristics from the REVEAL Registry. , 2010, Chest.

[6]  Sally H Vitali,et al.  Impaired Vasoconstriction and Nitric Oxide-Mediated Relaxation in Pulmonary Arteries of Hypoxia- and Monocrotaline-Induced Pulmonary Hypertensive Rats , 2010, Journal of Pharmacology and Experimental Therapeutics.

[7]  M. Frid,et al.  Sustained hypoxia leads to the emergence of cells with enhanced growth, migratory, and promitogenic potentials within the distal pulmonary artery wall. , 2009, American journal of physiology. Lung cellular and molecular physiology.

[8]  M. Maitland,et al.  Inflammation, growth factors, and pulmonary vascular remodeling. , 2009, Journal of the American College of Cardiology.

[9]  H. Farber.  The Status of Pulmonary Arterial Hypertension in 2008 , 2008, Circulation.

[10]  Meijing Wang,et al.  The effects of endogenous sex hormones and acute hypoxia on vasoconstriction in isolated rat pulmonary artery rings. , 2008, The Journal of surgical research.

[11]  D. Ingber,et al.  Absence of Cyclooxygenase-2 Exacerbates Hypoxia-Induced Pulmonary Hypertension and Enhances Contractility of Vascular Smooth Muscle Cells , 2008, Circulation.

[12]  V. Kurup,et al.  Pulmonary arterial remodeling induced by a Th2 immune response , 2008, The Journal of experimental medicine.

[13]  U. Ikeda,et al.  Interleukin-10 Expression Mediated by an Adeno-Associated Virus Vector Prevents Monocrotaline-Induced Pulmonary Arterial Hypertension in Rats , 2007, Circulation research.

[14]  U. Christians,et al.  Serotonin transporter protein in pulmonary hypertensive rats treated with atorvastatin. , 2007, American journal of physiology. Lung cellular and molecular physiology.

[15]  W. Seeger,et al.  Phosphodiesterase 1 Upregulation in Pulmonary Arterial Hypertension: Target for Reverse-Remodeling Therapy , 2007, Circulation.

[16]  Y. Shang,et al.  Transplantation of autologous endothelial progenitor cells may be beneficial in patients with idiopathic pulmonary arterial hypertension: a pilot randomized controlled trial. , 2007, Journal of the American College of Cardiology.

[17]  S. N. Murthy,et al.  Intratracheal mesenchymal stem cell administration attenuates monocrotaline-induced pulmonary hypertension and endothelial dysfunction. , 2007, American journal of physiology. Heart and circulatory physiology.

[18]  R. Barst,et al.  Treatment of pulmonary arterial hypertension with the selective endothelin-A receptor antagonist sitaxsentan. , 2006, Journal of the American College of Cardiology.

[19]  M. Frid,et al.  Hypoxia-induced pulmonary vascular remodeling requires recruitment of circulating mesenchymal precursors of a monocyte/macrophage lineage. , 2006, The American journal of pathology.

[20]  R. Jones,et al.  The influence of sex hormones on pulmonary vascular reactivity: possible vasodilator therapies for the treatment of pulmonary hypertension. , 2006, Current vascular pharmacology.

[21]  T. Welte,et al.  Goal-oriented treatment and combination therapy for pulmonary arterial hypertension , 2005, European Respiratory Journal.

[22]  W. Seeger,et al.  Reversal of experimental pulmonary hypertension by PDGF inhibition. , 2005, The Journal of clinical investigation.

[23]  M. Humbert,et al.  Long-Term Response to Calcium Channel Blockers in Idiopathic Pulmonary Arterial Hypertension , 2005, Circulation.

[24]  S. Archer,et al.  Gene therapy targeting survivin selectively induces pulmonary vascular apoptosis and reverses pulmonary arterial hypertension. , 2005, The Journal of clinical investigation.

[25]  Dexter L. Lee,et al.  Hypertension and RhoA/Rho-kinase signaling in the vasculature: highlights from the recent literature. , 2004, Hypertension.

[26]  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.

[27]  D. Mccrory,et al.  Prognosis of pulmonary arterial hypertension: ACCP evidence-based clinical practice guidelines. , 2004, Chest.

[28]  J. Krishnan,et al.  Pulmonary hypertension as a risk factor for death in patients with sickle cell disease. , 2004, The New England journal of medicine.

[29]  M. Gladwin,et al.  Pulmonary hypertension as a risk factor for death in patients with sickle cell disease. , 2004, The New England journal of medicine.

[30]  R. Khalil,et al.  Gender, sex hormones, and vascular tone. , 2004, American journal of physiology. Regulatory, integrative and comparative physiology.

[31]  R. Budhiraja,et al.  Endothelial Dysfunction in Pulmonary Hypertension , 2004, Circulation.

[32]  G. Berry,et al.  Simvastatin Rescues Rats From Fatal Pulmonary Hypertension by Inducing Apoptosis of Neointimal Smooth Muscle Cells , 2003, Circulation.

[33]  J. Dyck,et al.  Dichloroacetate, a Metabolic Modulator, Prevents and Reverses Chronic Hypoxic Pulmonary Hypertension in Rats: Role of Increased Expression and Activity of Voltage-Gated Potassium Channels , 2002, Circulation.

[34]  T. Minamino,et al.  Targeted expression of heme oxygenase-1 prevents the pulmonary inflammatory and vascular responses to hypoxia , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[35]  M. Yanagisawa,et al.  Endothelin B receptor deficiency potentiates ET-1 and hypoxic pulmonary vasoconstriction. , 2001, American journal of physiology. Lung cellular and molecular physiology.

[36]  R. Nagai,et al.  Vascular smooth muscle cell phenotypes in primary pulmonary hypertension. , 2001, The European respiratory journal.

[37]  R. Khalil,et al.  Gender-related distinctions in protein kinase C activity in rat vascular smooth muscle. , 2001, American journal of physiology. Cell physiology.

[38]  R. Trembath,et al.  Heterozygous germline mutations in BMPR2, encoding a TGF-β receptor, cause familial primary pulmonary hypertension , 2000, Nature Genetics.

[39]  J. Yuan,et al.  Hypoxic pulmonary vasoconstriction: role of voltage-gated potassium channels , 2000, Respiratory research.

[40]  Adrian M Heilbut,et al.  Complete reversal of fatal pulmonary hypertension in rats by a serine elastase inhibitor , 2000, Nature Medicine.

[41]  R. Khalil,et al.  Gender-specific reduction in contractility and [Ca(2+)](i) in vascular smooth muscle cells of female rat. , 2000, American journal of physiology. Cell physiology.

[42]  L. Shimoda,et al.  Altered pulmonary vasoreactivity in the chronically hypoxic lung. , 2000, Physiological research.

[43]  N. Voelkel,et al.  Pulmonary prostacyclin synthase overexpression in transgenic mice protects against development of hypoxic pulmonary hypertension. , 1999, The Journal of clinical investigation.

[44]  L. Kobzik,et al.  Hypoxia induces severe right ventricular dilatation and infarction in heme oxygenase-1 null mice. , 1999, The Journal of clinical investigation.

[45]  I. Godsland,et al.  17β-Oestradiol enhances release of matrix metalloproteinase-2 from human vascular smooth muscle cells , 1998 .

[46]  I. Godsland,et al.  17beta-oestradiol enhances release of matrix metalloproteinase-2 from human vascular smooth muscle cells. , 1998, Biochimica et biophysica acta.

[47]  C. Hsieh,et al.  Prevention of Hypoxia-Induced Pulmonary Hypertension by Enhancement of Endogenous Heme Oxygenase-1 in the Rat. • 238 , 1997, Pediatric Research.

[48]  R. McIntyre,et al.  Mechanistic imbalance of pulmonary vasomotor control in progressive lung injury. , 1996, Surgery.

[49]  S. Rich,et al.  The effect of high doses of calcium-channel blockers on survival in primary pulmonary hypertension. , 1992, The New England journal of medicine.

[50]  P. Braquet,et al.  Loss of endothelium-dependent relaxant activity in the pulmonary circulation of rats exposed to chronic hypoxia. , 1991, The Journal of clinical investigation.

[51]  B. Groves,et al.  Histopathology of primary pulmonary hypertension. A qualitative and quantitative study of pulmonary blood vessels from 58 patients in the National Heart, Lung, and Blood Institute, Primary Pulmonary Hypertension Registry. , 1989, Circulation.

[52]  M. Gillespie,et al.  Vascular hyperresponsiveness in perfused lungs from monocrotaline-treated rats. , 1986, The American journal of physiology.