Research Topics
Genomes and GenesSpecies | Munekazu YamakuchiSummaryAffiliation: Johns Hopkins University Country: USA Publications
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Publications
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...- 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... 
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...- 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... - 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... 
MicroRNA-34a regulation of endothelial senescenceTakashi Ito
Department of Medicine, Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, West Henrietta, NY 14586, USA
Biochem Biophys Res Commun 398:735-40. 2010..Our data suggest that miR-34a contributes to endothelial senescence through suppression of SIRT1...- 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... - 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... - 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... - 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... - 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... - 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... - 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... - 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... - 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... - 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... - 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... - 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... - Anandamide induces apoptosis in human endothelial cells: its regulation system and clinical implicationsKazuyo Yamaji
Department of Laboratory and Molecular Medicine, Faculty of Medicine, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8520, Japan
Thromb Haemost 89:875-84. 2003..In conclusion, we propose that AEA may play a crucial role in EC injury under conditions of shock, and that the use of inhibitors of the AEA regulation system may have a therapeutic effect under these conditions...