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Genomes and Genes | Charles J LowensteinSummaryAffiliation: Johns Hopkins University Country: USA Publications
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N-ethylmaleimide-sensitive factor: a redox sensor in exocytosisCharles J Lowenstein
Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Biol Chem 387:1377-83. 2006..Since radicals such as NO and H(2)O(2) inhibit NSF and decrease exocytosis, NSF may act as a redox sensor, modulating exocytosis in response to changes in oxidative stress...- Regulation of Weibel-Palade body exocytosisCharles J Lowenstein
Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
Trends Cardiovasc Med 15:302-8. 2005..This review examines the regulation of WPB exocytosis-the exocytic machinery, activators, and inhibitors of exocytosis-and speculates about the development of novel anti-exocytic drugs... 
Nitric oxide regulation of protein trafficking in the cardiovascular systemCharles J Lowenstein
The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Cardiovasc Res 75:240-6. 2007..NO regulation of vesicle trafficking is a molecular mechanism that explains some of the cardiovascular effects of NO, and may be of broad physiological significance...- iNOS (NOS2) at a glanceCharles J Lowenstein
Division of Cardiology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
J Cell Sci 117:2865-7. 2004 - Nitric oxide regulates exocytosis by S-nitrosylation of N-ethylmaleimide-sensitive factorKenji Matsushita
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Cell 115:139-50. 2003..NO may regulate exocytosis in a variety of physiological processes, including vascular inflammation, neurotransmission, thrombosis, and cytotoxic T lymphocyte cell killing... - Vascular endothelial growth factor regulation of Weibel-Palade-body exocytosisKenji Matsushita
Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Blood 105:207-14. 2005..Thus, VEGF plays a dual role in regulating endothelial exocytosis, triggering pathways that both promote and inhibit endothelial exocytosis. Regulation of endothelial exocytosis may explain part of the proinflammatory effects of VEGF... - Exocytosis of endothelial cells is regulated by N-ethylmaleimide-sensitive factorMunekazu Yamakuchi
Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD, USA
Methods Mol Biol 440:203-15. 2008..Further characterization of the factors that regulate exocytosis will lead to novel treatments for vascular diseases such as myocardial infarction and stroke... - Hydrogen peroxide regulation of endothelial exocytosis by inhibition of N-ethylmaleimide sensitive factorKenji Matsushita
Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
J Cell Biol 170:73-9. 2005..Increasing endogenous H(2)O(2) levels in mice decreases exocytosis and platelet rolling on venules in vivo. By inhibiting endothelial cell exocytosis, endogenous H(2)O(2) may protect the vasculature from inflammation and thrombosis... - HMG-CoA reductase inhibitors inhibit endothelial exocytosis and decrease myocardial infarct sizeMunekazu Yamakuchi
Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Circ Res 96:1185-92. 2005..These findings may explain part of the pleiotropic effects of statin therapy for patients with cardiovascular disease... - Aldosterone activates endothelial exocytosisYoungtae Jeong
Department of Medicine, Graduate Program in Pathobiology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 106:3782-7. 2009..Aldosterone antagonism may decrease vascular inflammation and cardiac fibrosis in part by blocking endothelial exocytosis... - Epigallocatechin gallate inhibits endothelial exocytosisMunekazu Yamakuchi
Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Biol Chem 389:935-41. 2008..NOS inhibition revealed that NO mediates the anti-inflammatory effects of EGCG. Our data suggest that polyphenols can decrease vascular inflammation by increasing the synthesis of NO, which blocks endothelial exocytosis... - Ceramide triggers Weibel-Palade body exocytosisRinky Bhatia
Division of Cardiology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Circ Res 95:319-24. 2004..These data suggest a novel mechanism by which ceramide induces vascular inflammation and thrombosis... - Increased endothelial exocytosis and generation of endothelin-1 contributes to constriction of aged arteriesAditya Goel
Department of Anesthesiology, Johns Hopkins University, Baltimore, MD 21205, USA
Circ Res 107:242-51. 2010..Circulating levels of endothelin (ET)-1 and endogenous ET(A)-mediated constriction are increased in human aging. The mechanisms responsible are not known... - P53-induced microRNA-107 inhibits HIF-1 and tumor angiogenesisMunekazu Yamakuchi
Department of Medicine, Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA
Proc Natl Acad Sci U S A 107:6334-9. 2010..Finally, in human colon cancer specimens, expression of miR-107 is inversely associated with expression of HIF-1beta. Taken together these data suggest that miR-107 can mediate p53 regulation of hypoxic signaling and tumor angiogenesis... - Regulation of platelet granule exocytosis by S-nitrosylationCraig N Morrell
Department of Comparative Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 102:3782-7. 2005..Platelets lacking endothelial NO synthase show increased rolling on venules, increased thrombosis in arterioles, and increased exocytosis in vivo. Regulation of exocytosis is thus a mechanism by which NO regulates thrombosis... - Antibody to human leukocyte antigen triggers endothelial exocytosisMunekazu Yamakuchi
Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 104:1301-6. 2007..Our data show that antibody to host antigens can activate human endothelial cell exocytosis and leukocyte trafficking. By triggering vascular inflammation, antibody activation of exocytosis may play a role in transplant rejection... - Sphingosine 1-phosphate activates Weibel-Palade body exocytosisKenji Matsushita
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 101:11483-7. 2004..Thus S1P plays a dual role in regulating endothelial exocytosis, triggering pathways that both promote and inhibit endothelial exocytosis. Regulation of endothelial exocytosis may explain part of the proinflammatory effects of S1P... - MicroRNA-126 regulates endothelial expression of vascular cell adhesion molecule 1Tamia A Harris
Cellular and Molecular Medicine Program and Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 105:1516-21. 2008..These data suggest that microRNA can regulate adhesion molecule expression and may provide additional control of vascular inflammation... - Nitric oxide inhibits exocytosis of cytolytic granules from lymphokine-activated killer cellsMarcella Ferlito
Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 103:11689-94. 2006..Our data suggest that Ras mediates NO inhibition of lymphocyte cytotoxicity and emphasize that alterations in the cellular redox state may regulate the exocytic signaling pathway... - miR-34a repression of SIRT1 regulates apoptosisMunekazu Yamakuchi
Departments of Medicine and Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 105:13421-6. 2008..Finally, miR-34a itself is a transcriptional target of p53, suggesting a positive feedback loop between p53 and miR-34a. Thus, miR-34a functions as a tumor suppressor, in part, through a SIRT1-p53 pathway... - A novel inhibitor of N-ethylmaleimide-sensitive factor decreases leukocyte trafficking and peritonitisCraig N Morrell
Department of Comparative Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD, USA
J Pharmacol Exp Ther 314:155-61. 2005..These data suggest that NSF is a critical regulator of leukocyte trafficking in vivo. Novel compounds that inhibit the exocytic machinery in endothelial cells may be useful anti-inflammatory drugs... - Ets-1 and Ets-2 regulate the expression of microRNA-126 in endothelial cellsTamia A Harris
Cellular and Molecular Medicine Program, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
Arterioscler Thromb Vasc Biol 30:1990-7. 2010..MicroRNA-126 (miR-126) is highly expressed in endothelial cells, and it regulates angiogenesis and vascular inflammation. Here we show that the transcription factors Ets-1 and Ets-2 regulate miR-126 expression... - Inhibition of N-ethylmaleimide-sensitive factor protects against myocardial ischemia/reperfusion injuryJohn W Calvert
Department of Medicine, Division of Cardiology and Department of Pathology, Albert Einstein College of Medicine, Bronx, NY, USA
Circ Res 101:1247-54. 2007..These data suggest that drugs targeting endothelial exocytosis may be useful in the treatment of myocardial injury following ischemia/reperfusion... - VAMP-1, VAMP-2, and syntaxin-4 regulate ANP release from cardiac myocytesMarcella Ferlito
Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
J Mol Cell Cardiol 49:791-800. 2010..Our data suggest that three specific SNAREs regulate cardiac myocyte exocytosis of ANP. Pathways that modify the exocytic machinery may influence natriuresis and blood pressure... - Acetylation of mitogen-activated protein kinase phosphatase-1 inhibits Toll-like receptor signalingWangsen Cao
Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
J Exp Med 205:1491-503. 2008..Our data suggest that acetylation of MKP-1 inhibits innate immune signaling. This pathway may be an important therapeutic target in the treatment of inflammatory diseases... - Nitric oxide inhibits the adenovirus proteinase in vitro and viral infectivity in vivoWangsen Cao
Division of Cardiology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
FASEB J 17:2345-6. 2003..These data suggest that NO may be a useful antiviral agent against viruses encoding a cysteine proteinase and in particular may be an antiadenovirus agent... - Peroxynitrite inhibition of Coxsackievirus infection by prevention of viral RNA entryElizaveta Padalko
Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 101:11731-6. 2004..These data suggest that peroxynitrite is an endogenous effector of the immune response to viruses... - A novel class of fusion polypeptides inhibits exocytosisKenji Matsushita
Department of Medicine, The Johns Hopkins University School of Medicine, 950 Ross Building, 720 Rutland Avenue, Baltimore, MD 21205, USA
Mol Pharmacol 67:1137-44. 2005..These TAT-NSF compounds may be useful in the treatment of a variety of diseases in which exocytosis plays a prominent role, including myocardial infarction, stroke, thrombosis, and autoimmune disorders... 
High-density lipoprotein metabolism and endothelial functionCharles J Lowenstein
Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642, USA
Curr Opin Endocrinol Diabetes Obes 17:166-70. 2010..High-density lipoprotein (HDL) protects against atherosclerosis, transporting cholesterol from peripheral cells to the liver, where it is excreted into the bile. However, HDL also has prominent vascular protective effects...- Outbreak management and implications of a nosocomial norovirus outbreakCecilia P Johnston
Division of Infectious Diseases, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA
Clin Infect Dis 45:534-40. 2007..We describe a norovirus outbreak and its control in a tertiary care hospital during February-May 2004... - MiR-34, SIRT1 and p53: the feedback loopMunekazu Yamakuchi
Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
Cell Cycle 8:712-5. 2009..Based on this observation, we propose a positive feedback loop, in which p53 induces expression of miR-34a which suppresses SIRT1, increasing p53 activity... - Glutamate mediates platelet activation through the AMPA receptorCraig N Morrell
Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
J Exp Med 205:575-84. 2008..Importantly, mice lacking GluR1 have a prolonged time to thrombosis in vivo. Our data identify glutamate as a regulator of platelet activation, and suggest that the AMPA receptor is a novel antithrombotic target... - Inducible nitric oxide synthase expression inhibition by adenovirus E1AWangsen Cao
Division of Cardiology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 100:7773-8. 2003..E1A is thus able to deactivate a critical component of the host defense against viral infection. Viral inhibition of NO production is a mechanism that may enable certain viruses to evade the host innate immune system... - Glutamate excitotoxicity mediates neuronal apoptosis after hypothermic circulatory arrestElaine E Tseng
Division of Cardiac Surgery, Johns Hopkins Medical Institutions, Baltimore, Maryland, USA
Ann Thorac Surg 89:440-5. 2010..This study was undertaken to determine whether glutamate receptor antagonism reduces nitric oxide formation and neuronal apoptosis after hypothermic circulatory arrest... - Purification and assessment of proteins associated with nitric oxide synthaseCharles J Lowenstein
Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
Methods Enzymol 353:233-40. 2002 - Gene therapy with inducible nitric oxide synthase protects against myocardial infarction via a cyclooxygenase-2-dependent mechanismQianhong Li
Division of Cardiology, University of Louisville, The Jewish Hospital Heart and Lung Institute, Louisville, KY 40292, USA
Circ Res 92:741-8. 2003..We propose that iNOS and COX-2 form a stress-responsive functional module that mitigates ischemia/reperfusion injury... - Novel pathogenetic mechanisms in myocarditis: nitric oxide signalingMichelle M Kittleson
The Johns Hopkins Medical Institutions, Baltimore, MD 21205, USA
Heart Fail Clin 1:345-61. 2005 - Transactivation of miR-34a by p53 broadly influences gene expression and promotes apoptosisTsung Cheng Chang
The McKusick Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Mol Cell 26:745-52. 2007..Therefore, it is likely that an important function of miR-34a is the modulation and fine-tuning of the gene expression program initiated by p53... - What's in a name? eNOS and anaphylactic shockCharles J Lowenstein
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, and Cardiovascular Division, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
J Clin Invest 116:2075-8. 2006..in anaphylaxis necessarily exerting its effect solely in the vascular endothelium, or might this "endothelial enzyme" actually be playing a more fundamental role in an entirely different tissue? After all, what's in a name?.. - Measuring reactive oxygen species inhibition of endothelin-converting enzymeCharles J Lowenstein
Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
Methods Enzymol 353:263-8. 2002 - TIMAP, a novel CAAX box protein regulated by TGF-beta1 and expressed in endothelial cellsWangsen Cao
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
Am J Physiol Cell Physiol 283:C327-37. 2002..Hence, TIMAP is a novel gene highly expressed in endothelial and hematopoietic cells and regulated by TGF-beta1. On the basis of its domain structure, TIMAP may serve a signaling function, potentially through interaction with PP1... - Pathogen recognition by Toll-like receptor 2 activates Weibel-Palade body exocytosis in human aortic endothelial cellsTakeshi Into
Department of Oral Disease Research, National Institute for Longevity Sciences, National Center for Geriatrics and Gerontology, 36 3 Gengo, Morioka, Obu, Aichi 474 8522, Japan
J Biol Chem 282:8134-41. 2007.... - Smad2 mediates transforming growth factor-beta induction of endothelial nitric oxide synthase expressionMarta Saura
Department of Physiology, Universidad de Alcal, Madrid, Spain
Circ Res 91:806-13. 2002..Because Smad2 can interact with a variety of transcription factors, coactivators, and corepressors, Smad2 may thus act as an integrator of multiple signals in the regulation of eNOS expression... - Viral protease cleavage of inhibitor of kappaBalpha triggers host cell apoptosisCarlos Zaragoza
Fundación Centro Nacional de Investigaciones Cardiovasculares, Melchor Fernandez Almagro 3, 28029 Madrid, Spain
Proc Natl Acad Sci U S A 103:19051-6. 2006..IkappaBalpha thus acts as a sensor of viral infection. Cleavage of host proteins by pathogen proteases is a novel mechanism by which the host recognizes and responds to viral infection... - Nitric oxide signaling comes of age: 20 years and thrivingSantiago Lamas
Cardiovasc Res 75:207-9. 2007 - Rac1 regulates the release of Weibel-Palade Bodies in human aortic endothelial cellsShui Xiang Yang
Cardiovascular Center, Tongren Hospital, Capital University of Medical Sciences, Beijing 100730, China
Chin Med J (Engl) 117:1143-50. 2004..But the signal transduction pathway leading to WPB release is not yet defined. We hypothesized that small G-protein rac1 and reactive oxygen species (ROS) mediate the ligand induced release of Weibel-Palade Bodies... - Exogenous thioredoxin reduces inflammation in autoimmune myocarditisCharles J Lowenstein
Circulation 110:1178-9. 2004 - Myocardial reperfusion injuryCharles J Lowenstein
N Engl J Med 357:2409; author reply 2409-10. 2007 - Nitric oxide regulates vascular calcification by interfering with TGF- signallingYosuke Kanno
Department of Oral Disease Research, National Center for Geriatrics and Gerontology, 36 3 Gengo, Morioka cho, Obu, Aichi 474 8511, Japan
Cardiovasc Res 77:221-30. 2008..Nitric oxide (NO) is crucial for maintaining vascular function, but little is known about how NO affects vascular calcification. The aim of this study was to examine the effect of NO on vascular calcification... - Inhibitor of NF kappa B alpha is a host sensor of coxsackievirus infectionMarta Saura
Departamento de Fisiologia, Facultad de Medicina, Universidad de Alcala, Alcala de Henares, Spain
Cell Cycle 6:503-6. 2007..IkBalpha thus acts as a sensor of viral infection. Cleavage of host proteins by pathogen proteases is a novel mechanism by which the host recognizes and responds to viral infection... - Mature hepatocyte growth factor/scatter factor on the surface of human granulocytes is released by a mechanism involving activated factor XaTomokazu Ohnishi
Division of Biochemistry and Molecular Dentistry, Department of Developmental Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Sakuragaoka, Kagoshima, Japan
J Immunol 176:6945-53. 2006..Thus, human granulocytes may function as a transporter of HGF in the peripheral blood, releasing HGF at the injured sites caused by blood coagulation, where HGF may promote tissue repair... - Stat3 mediates interleukin-6 [correction of interelukin-6] inhibition of human endothelial nitric-oxide synthase expressionMarta Saura
Department of Physiology, Universidad de Alcala, Alcala de Henares, 28871 Madrid, Spain
J Biol Chem 281:30057-62. 2006..Our data show that IL-6 has direct effects upon endothelial cells, inhibiting eNOS expression in part through Stat3. Decreased levels of eNOS may be an important component of the pro-atherogenic effect of the APR...