scholarly journals The Role of p38 MAPK in Rheumatic Diseases

2015 ◽  
Vol 3 (2) ◽  
Author(s):  
Athanasios Mavropoulos ◽  
Andreas L. Koutsoumpas ◽  
Dimitrios P. Bogdanos
Keyword(s):  
P38 Mapk ◽  
2008 ◽  
Vol 56 (1) ◽  
pp. 83-89 ◽  
Author(s):  
Ewa Jablonska ◽  
Wioletta Ratajczak ◽  
Jakub Jablonski

2010 ◽  
Vol 30 (3) ◽  
pp. 250-253
Author(s):  
Jian-ming WNAG ◽  
De-yi ZHENG ◽  
Yi-tao JIA ◽  
Jin-feng FU ◽  
Xing-feng ZHENG ◽  
...  

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1277.3-1278
Author(s):  
T. Oton ◽  
L. Carmona ◽  
J. L. Andréu Sánchez

Background:Methotrexate (MTX) is currently a mainstream drug in the treatment of rheumatic diseases. However, the response to MTX is not universal and may be conditioned by a number of factors, among which adherence could be crucial.Objectives:The aim of this study is to explore adherence to MTX in patients with rheumatic diseases, facilitators and perceived when taking and maintaining the prescription.Methods:A qualitative study of content analysis was performed. Focus groups with patients taking either oral or subcutaneous MTX (being the main or coadjuvant treatment) for any rheumatic disease was performed. The groups were moderated by a rheumatologist that was unknown for the patients. The speech was recorded and transcribed. Subsequently, an inductive coding was performed with the help of Atlas.ti and main themes and sub-themes were extracted, with examples of verbatim anonymized speech.Results:Three focus groups were conducted, with a total of 12 participants, of whom eight were women, seven had rheumatoid arthritis, three had psoriatic arthritis, one had spondyloarthritis, and one had systemic lupus erythematosus. All patients reported an adequate adherence to treatment. The barriers identified were: information in the leaflet, technical language in the consults, difficult access to doctor´s appointment, social environment, side effects and the subcutaneous device. As facilitators, the following aspects were discussed: good predisposition of the physician, reliable graphic information, role of associations and partners support.The unmet needs detected were: problems with travelling, protocols for eventualities, absence of a plan of care, neglection of “non-physical” symptoms, disinformation on side effects and training in complementary aspects.Conclusion:Getting reliable information was the main barrier identified. The environment and side effects may also negatively impact on adherence. Shared decision making is a goal to be achieved in the future in these patients.Disclosure of Interests:Teresa Oton Consultant of: Novartis Farmaceutica, SA, Pfizer, S.L.U., Merck Sharp & Dohme España, S.A., Roche Farma, S.A, Sanofi Aventis, AbbVie Spain, S.L.U., and Laboratorios Gebro Pharma, SA (All trhough institution), Loreto Carmona Grant/research support from: Novartis Farmaceutica, SA, Pfizer, S.L.U., Merck Sharp & Dohme España, S.A., Roche Farma, S.A, Sanofi Aventis, AbbVie Spain, S.L.U., and Laboratorios Gebro Pharma, SA (All trhough institution), José Luis Andréu Sánchez: None declared


2007 ◽  
Vol 282 (38) ◽  
pp. 27713-27720 ◽  
Author(s):  
Mete Erdogan ◽  
Ambra Pozzi ◽  
Neil Bhowmick ◽  
Harold L Moses ◽  
Roy Zent

TC21(R-Ras2), a Ras-related GTPase with transforming potential similar to H-, K- and N-Ras, is implicated in the pathogenesis of human cancers. Transforming growth factor β (TGF-β), a cytokine that plays a significant role in modulating tumorigenesis, normally prevents uncontrolled cell proliferation but paradoxically induces proliferation in H-Ras-transformed cancer cells. Although TC21 activates some pathways that mediate cellular transformation by the classical Ras proteins, the mechanisms through which TC21 induces tumor formation and how TGF-β regulates TC21 transformed cells is not known. To better understand the role of TC21 in cancer progression, we overexpressed an activated G23V mutant of TC21 in a nontumorigenic murine mammary epithelial (EpH4) cell line. Mutant TC21-expressing cells were significantly more oncogenic than cells expressing activated G12V H-Ras both in vivo and in vitro. TC21-induced transformation and proliferation required activation of p38 MAPK, mTOR (the mammalian target of rapamycin), and phosphoinositide 3-kinase but not Akt/PKB. Transformation by TC21 rendered EpH4 cells insensitive to the growth inhibitory effects of TGF-β, and the soft agar growth of these cells was increased upon TGF-β stimulation. Despite losing responsiveness to TGF-β-mediated growth inhibition, both Smad-dependent and independent pathways remained intact in TC21-transformed cells. Thus, overexpression of active TC21 in EpH4 cells induces tumorigenicity through the phosphoinositide 3-kinase, p38 MAPK, and mTOR pathways, and these cells lose their sensitivity to the normal growth inhibitory role of TGF-β.


2003 ◽  
Vol 979 (1-2) ◽  
pp. 98-103 ◽  
Author(s):  
Shaji Philip ◽  
William M. Armstead
Keyword(s):  

PLoS ONE ◽  
2013 ◽  
Vol 8 (10) ◽  
pp. e75356 ◽  
Author(s):  
Chern Chiuh Woo ◽  
Annie Hsu ◽  
Alan Prem Kumar ◽  
Gautam Sethi ◽  
Kwong Huat Benny Tan

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