Transient silencing of transforming growth factor‐β1 expression restores nitric oxide generation in diabetic hematopoietic stem/progenitor cells: Role of thrombospondin‐1.

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Jesmin Jahan ◽  
Duran Miguel ◽  
Julio Quiroz ◽  
Charles Gracia ◽  
Stephen Bartelmez ◽  
...  
2002 ◽  
Vol 122 (4) ◽  
pp. 1122-1132 ◽  
Author(s):  
Xavier Bessa ◽  
J.Ignasi Elizalde ◽  
Francesc Mitjans ◽  
Virgínia Piñol ◽  
Rosa Miquel ◽  
...  

2015 ◽  
Vol 42 (6) ◽  
pp. 943-947 ◽  
Author(s):  
Takahisa Suzuki ◽  
Naoki Iwamoto ◽  
Satoshi Yamasaki ◽  
Ayako Nishino ◽  
Yoshikazu Nakashima ◽  
...  

Objective.To investigate the role of thrombospondin 1 (TSP-1) in RA.Methods.Expression of TSP-1 in synovial tissues was determined by immunohistochemistry. Expression of TSP-1 in rheumatoid fibroblast-like synovial cells (FLS) was investigated by quantitative real-time PCR and ELISA. Correlations among the plasma TSP-1 and other variables in patients with RA were examined.Results.Expression of TSP-1 was increased in rheumatoid synovial tissues. Transforming growth factor-β1 (TGF-β1) clearly increased TSP-1 expression in FLS on both mRNA and protein levels. Changes in plasma TSP-1 were associated with those in 28-joint Disease Activity Score-erythrocyte sedimentation rate and plasma TGF-β1.Conclusion.TSP-1 might be critically involved in the disease process of RA through the TGF-β1/TSP-1 axis.


Hypertension ◽  
2000 ◽  
Vol 35 (1) ◽  
pp. 86-90 ◽  
Author(s):  
Masamichi Koyanagi ◽  
Kensuke Egashira ◽  
Mayuko Kubo-Inoue ◽  
Makoto Usui ◽  
Shiro Kitamoto ◽  
...  

2009 ◽  
Vol 17 (4) ◽  
pp. 578-588 ◽  
Author(s):  
Mallikarjuna Reddy Metukuri ◽  
Rajaie Namas ◽  
Chase Gladstone ◽  
Thierry Clermont ◽  
Bahiyya Jefferson ◽  
...  

Blood ◽  
2011 ◽  
Vol 117 (1) ◽  
pp. 246-249 ◽  
Author(s):  
Solène Evrard ◽  
Olivier Bluteau ◽  
Micheline Tulliez ◽  
Philippe Rameau ◽  
Patrick Gonin ◽  
...  

Abstract Transforming growth factor-β1 (TGF-β1) is the most important cytokine involved in the promotion of myelofibrosis. Mechanisms leading to its local activation in the bone marrow environment remain unclear. As a recent study has highlighted the role of thrombospondin-1 (TSP-1) in platelet-derived TGF-β1 activation, we investigated the role of TSP-1 in the TPOhigh murine model of myelofibrosis. Two groups of engrafted mice, WT TPOhigh and Tsp-1–null TPOhigh, were constituted. All mice developed a similar myeloproliferative syndrome and an increase in total TGF-β1 levels in the plasma and in extracellular fluids of marrow and spleen. Surprisingly, we were able to detect the active form of TGF-β1 in Tsp-1–null TPOhigh mice. Accordingly, these mice developed marrow and spleen fibrosis, with intriguingly a higher grade than in WT TPOhigh mice. Our results show that TSP-1 is not the major activator of TGF-β1 in TPO-induced myelofibrosis, suggesting the contribution of another mechanism in the megakaryocyte/platelet compartment.


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