Charles J Lowenstein

Summary

Affiliation: Johns Hopkins University
Country: USA

Publications

  1. pmc Hydrogen peroxide regulation of endothelial exocytosis by inhibition of N-ethylmaleimide sensitive factor
    Kenji Matsushita
    Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    J Cell Biol 170:73-9. 2005
  2. ncbi request reprint N-ethylmaleimide-sensitive factor: a redox sensor in exocytosis
    Charles J Lowenstein
    Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Biol Chem 387:1377-83. 2006
  3. pmc Nitric oxide regulation of protein trafficking in the cardiovascular system
    Charles J Lowenstein
    The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Cardiovasc Res 75:240-6. 2007
  4. ncbi request reprint Regulation of Weibel-Palade body exocytosis
    Charles J Lowenstein
    Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Trends Cardiovasc Med 15:302-8. 2005
  5. ncbi request reprint iNOS (NOS2) at a glance
    Charles 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
  6. pmc Nitric oxide regulates exocytosis by S-nitrosylation of N-ethylmaleimide-sensitive factor
    Kenji Matsushita
    Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Cell 115:139-50. 2003
  7. pmc Vascular endothelial growth factor regulation of Weibel-Palade-body exocytosis
    Kenji Matsushita
    Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Blood 105:207-14. 2005
  8. pmc Exocytosis of endothelial cells is regulated by N-ethylmaleimide-sensitive factor
    Munekazu Yamakuchi
    Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Methods Mol Biol 440:203-15. 2008
  9. ncbi request reprint Ceramide triggers Weibel-Palade body exocytosis
    Rinky Bhatia
    Division of Cardiology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Circ Res 95:319-24. 2004
  10. ncbi request reprint HMG-CoA reductase inhibitors inhibit endothelial exocytosis and decrease myocardial infarct size
    Munekazu Yamakuchi
    Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Circ Res 96:1185-92. 2005

Detail Information

Publications52

  1. pmc Hydrogen peroxide regulation of endothelial exocytosis by inhibition of N-ethylmaleimide sensitive factor
    Kenji 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...
  2. ncbi request reprint N-ethylmaleimide-sensitive factor: a redox sensor in exocytosis
    Charles 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...
  3. pmc Nitric oxide regulation of protein trafficking in the cardiovascular system
    Charles 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...
  4. ncbi request reprint Regulation of Weibel-Palade body exocytosis
    Charles 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...
  5. ncbi request reprint iNOS (NOS2) at a glance
    Charles 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
  6. pmc Nitric oxide regulates exocytosis by S-nitrosylation of N-ethylmaleimide-sensitive factor
    Kenji 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...
  7. pmc Vascular endothelial growth factor regulation of Weibel-Palade-body exocytosis
    Kenji 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...
  8. pmc Exocytosis of endothelial cells is regulated by N-ethylmaleimide-sensitive factor
    Munekazu 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...
  9. ncbi request reprint Ceramide triggers Weibel-Palade body exocytosis
    Rinky 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...
  10. ncbi request reprint HMG-CoA reductase inhibitors inhibit endothelial exocytosis and decrease myocardial infarct size
    Munekazu 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...
  11. pmc Epigallocatechin gallate inhibits endothelial exocytosis
    Munekazu 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...
  12. pmc Aldosterone activates endothelial exocytosis
    Youngtae 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...
  13. pmc Regulation of platelet granule exocytosis by S-nitrosylation
    Craig 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...
  14. pmc Antibody to human leukocyte antigen triggers endothelial exocytosis
    Munekazu 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...
  15. pmc Increased endothelial exocytosis and generation of endothelin-1 contributes to constriction of aged arteries
    Aditya 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...
  16. pmc Sphingosine 1-phosphate activates Weibel-Palade body exocytosis
    Kenji 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...
  17. pmc P53-induced microRNA-107 inhibits HIF-1 and tumor angiogenesis
    Munekazu 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...
  18. ncbi request reprint A novel inhibitor of N-ethylmaleimide-sensitive factor decreases leukocyte trafficking and peritonitis
    Craig 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...
  19. pmc Nitric oxide inhibits exocytosis of cytolytic granules from lymphokine-activated killer cells
    Marcella 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...
  20. pmc MicroRNA-126 regulates endothelial expression of vascular cell adhesion molecule 1
    Tamia 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...
  21. pmc miR-34a repression of SIRT1 regulates apoptosis
    Munekazu 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...
  22. pmc A novel class of fusion polypeptides inhibits exocytosis
    Kenji 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...
  23. pmc Ets-1 and Ets-2 regulate the expression of microRNA-126 in endothelial cells
    Tamia 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...
  24. pmc Inhibition of N-ethylmaleimide-sensitive factor protects against myocardial ischemia/reperfusion injury
    John 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...
  25. pmc VAMP-1, VAMP-2, and syntaxin-4 regulate ANP release from cardiac myocytes
    Marcella 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...
  26. pmc Acetylation of mitogen-activated protein kinase phosphatase-1 inhibits Toll-like receptor signaling
    Wangsen 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...
  27. pmc Peroxynitrite inhibition of Coxsackievirus infection by prevention of viral RNA entry
    Elizaveta 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...
  28. ncbi request reprint Nitric oxide inhibits the adenovirus proteinase in vitro and viral infectivity in vivo
    Wangsen 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...
  29. doi request reprint High-density lipoprotein metabolism and endothelial function
    Charles 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...
  30. ncbi request reprint Outbreak management and implications of a nosocomial norovirus outbreak
    Cecilia 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...
  31. ncbi request reprint MiR-34, SIRT1 and p53: the feedback loop
    Munekazu 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...
  32. pmc Glutamate mediates platelet activation through the AMPA receptor
    Craig 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...
  33. pmc Transactivation of miR-34a by p53 broadly influences gene expression and promotes apoptosis
    Tsung 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...
  34. pmc Glutamate excitotoxicity mediates neuronal apoptosis after hypothermic circulatory arrest
    Elaine 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...
  35. pmc Inducible nitric oxide synthase expression inhibition by adenovirus E1A
    Wangsen 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...
  36. pmc Gene therapy with inducible nitric oxide synthase protects against myocardial infarction via a cyclooxygenase-2-dependent mechanism
    Qianhong 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...
  37. ncbi request reprint Purification and assessment of proteins associated with nitric oxide synthase
    Charles J Lowenstein
    Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Methods Enzymol 353:233-40. 2002
  38. ncbi request reprint Novel pathogenetic mechanisms in myocarditis: nitric oxide signaling
    Michelle M Kittleson
    The Johns Hopkins Medical Institutions, Baltimore, MD 21205, USA
    Heart Fail Clin 1:345-61. 2005
  39. ncbi request reprint Measuring reactive oxygen species inhibition of endothelin-converting enzyme
    Charles J Lowenstein
    Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Methods Enzymol 353:263-8. 2002
  40. pmc What's in a name? eNOS and anaphylactic shock
    Charles 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?..
  41. ncbi request reprint TIMAP, a novel CAAX box protein regulated by TGF-beta1 and expressed in endothelial cells
    Wangsen 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...
  42. ncbi request reprint Pathogen recognition by Toll-like receptor 2 activates Weibel-Palade body exocytosis in human aortic endothelial cells
    Takeshi 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
    ....
  43. ncbi request reprint Smad2 mediates transforming growth factor-beta induction of endothelial nitric oxide synthase expression
    Marta Saura
    Department of Physiology, Universidad de Alcala, 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...
  44. pmc Viral protease cleavage of inhibitor of kappaBalpha triggers host cell apoptosis
    Carlos Zaragoza
    FundaciĆ³n 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...
  45. ncbi request reprint Nitric oxide signaling comes of age: 20 years and thriving
    Santiago Lamas
    Cardiovasc Res 75:207-9. 2007
  46. ncbi request reprint Rac1 regulates the release of Weibel-Palade Bodies in human aortic endothelial cells
    Shui 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...
  47. ncbi request reprint Nitric oxide regulates vascular calcification by interfering with TGF- signalling
    Yosuke 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...
  48. ncbi request reprint Mature hepatocyte growth factor/scatter factor on the surface of human granulocytes is released by a mechanism involving activated factor Xa
    Tomokazu 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...
  49. ncbi request reprint Myocardial reperfusion injury
    Charles J Lowenstein
    N Engl J Med 357:2409; author reply 2409-10. 2007
  50. ncbi request reprint Inhibitor of NF kappa B alpha is a host sensor of coxsackievirus infection
    Marta 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...
  51. ncbi request reprint Exogenous thioredoxin reduces inflammation in autoimmune myocarditis
    Charles J Lowenstein
    Circulation 110:1178-9. 2004
  52. ncbi request reprint Stat3 mediates interleukin-6 [correction of interelukin-6] inhibition of human endothelial nitric-oxide synthase expression
    Marta 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...