scholarly journals The autocrine role of tryptase in pressure overload-induced mast cell activation, chymase release and cardiac fibrosis

2016 ◽  
Vol 10 ◽  
pp. 16-23 ◽  
Author(s):  
Jianping Li ◽  
Shaiban Jubair ◽  
Scott P. Levick ◽  
Joseph S. Janicki
2009 ◽  
Vol 124 (4) ◽  
pp. 827-833.e2 ◽  
Author(s):  
Ken Fukuda ◽  
Masaharu Ohbayashi ◽  
Kei Morohoshi ◽  
Lane Zhang ◽  
Fu-Tong Liu ◽  
...  

2020 ◽  
Vol 1867 (4) ◽  
pp. 118622
Author(s):  
Anne Simonowski ◽  
Thomas Wilhelm ◽  
Pardes Habib ◽  
Carolin N. Zorn ◽  
Michael Huber

2008 ◽  
Vol 76 (7) ◽  
pp. 912-921 ◽  
Author(s):  
Montserrat Buceta ◽  
Eduardo Domínguez ◽  
Marián Castro ◽  
José Brea ◽  
David Álvarez ◽  
...  

Critical Care ◽  
10.1186/cc776 ◽  
2000 ◽  
Vol 4 (Suppl 1) ◽  
pp. P56
Author(s):  
A Walther ◽  
N Yilmaz ◽  
W Schmidt ◽  
A Secchi ◽  
MM Gebhard ◽  
...  

2017 ◽  
Vol 114 (8) ◽  
pp. E1490-E1499 ◽  
Author(s):  
Cristina Leoni ◽  
Sara Montagner ◽  
Andrea Rinaldi ◽  
Francesco Bertoni ◽  
Sara Polletti ◽  
...  

DNA methylation and specifically the DNA methyltransferase enzyme DNMT3A are involved in the pathogenesis of a variety of hematological diseases and in regulating the function of immune cells. Although altered DNA methylation patterns and mutations inDNMT3Acorrelate with mast cell proliferative disorders in humans, the role of DNA methylation in mast cell biology is not understood. By using mast cells lackingDnmt3a, we found that this enzyme is involved in restraining mast cell responses to acute and chronic stimuli, both in vitro and in vivo. The exacerbated mast cell responses observed in the absence ofDnmt3awere recapitulated or enhanced by treatment with the demethylating agent 5-aza-2′-deoxycytidine as well as by down-modulation ofDnmt1expression, further supporting the role of DNA methylation in regulating mast cell activation. Mechanistically, these effects were in part mediated by the dysregulated expression of the scaffold protein IQGAP2, which is characterized by the ability to regulate a wide variety of biological processes. Altogether, our data demonstrate that DNMT3A and DNA methylation are key modulators of mast cell responsiveness to acute and chronic stimulation.


Blood ◽  
2013 ◽  
Vol 121 (8) ◽  
pp. 1285-1295 ◽  
Author(s):  
Sophie Georgin-Lavialle ◽  
Ludovic Lhermitte ◽  
Patrice Dubreuil ◽  
Marie-Olivia Chandesris ◽  
Olivier Hermine ◽  
...  

Abstract Mast cell leukemia (MCL) is a very rare form of aggressive systemic mastocytosis accounting for < 1% of all mastocytosis. It may appear de novo or secondary to previous mastocytosis and shares more clinicopathologic aspects with systemic mastocytosis than with acute myeloid leukemia. Symptoms of mast cell activation—involvement of the liver, spleen, peritoneum, bones, and marrow—are frequent. Diagnosis is based on the presence of ≥ 20% atypical mast cells in the marrow or ≥ 10% in the blood; however, an aleukemic variant is frequently encountered in which the number of circulating mast cells is < 10%. The common phenotypic features of pathologic mast cells encountered in most forms of mastocytosis are unreliable in MCL. Unexpectedly, non-KIT D816V mutations are frequent and therefore, complete gene sequencing is necessary. Therapy usually fails and the median survival time is < 6 months. The role of combination therapies and bone marrow transplantation needs further investigation.


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