Proteomic analysis of chondromodulin-I-induced differentiation of mesenchymal stem cells into chondrocytes

2017 ◽  
Vol 159 ◽  
pp. 1-18 ◽  
Author(s):  
Shuang-chun Xing ◽  
Lian-xin Du ◽  
Wei Zhou ◽  
Yu-qiang Hu ◽  
Ya Feng ◽  
...  
PLoS ONE ◽  
2014 ◽  
Vol 9 (5) ◽  
pp. e97026 ◽  
Author(s):  
Dandan Ma ◽  
Li Cui ◽  
Jie Gao ◽  
Wenjuan Yan ◽  
Ying Liu ◽  
...  

Author(s):  
Vitor Marcel Faça ◽  
Maristela Delgado Orellana ◽  
Lewis Joel Greene ◽  
Dimas Tadeu Covas

Author(s):  
Galya Ivanova ◽  
Tiago Pereira ◽  
Ana Rita Caseiro ◽  
Petra Georgieva ◽  
Ana Colette Maurício

PLoS ONE ◽  
2017 ◽  
Vol 12 (3) ◽  
pp. e0174303 ◽  
Author(s):  
Alfonso Eirin ◽  
Xiang-Yang Zhu ◽  
Amrutesh S. Puranik ◽  
John R. Woollard ◽  
Hui Tang ◽  
...  

2012 ◽  
Vol 64 (5) ◽  
pp. 563-575 ◽  
Author(s):  
Balasundari Ramesh ◽  
Dillip Kumar Bishi ◽  
Suneel Rallapalli ◽  
Sarasabarathi Arumugam ◽  
Kotturathu Mammen Cherian ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Izuagie Attairu Ikhapoh ◽  
Christopher J. Pelham ◽  
Devendra K. Agrawal

Coronary artery stenting or angioplasty procedures frequently result in long-term endothelial dysfunction or loss and complications including arterial thrombosis and myocardial infarction. Stem cell-based therapies have been proposed to support endothelial regeneration. Mesenchymal stem cells (MSCs) differentiate into endothelial cells (ECs) in the presence of VEGF-Ain vitro. Application of VEGF-A and MSC-derived ECs at the interventional site is a complex clinical challenge. In this study, we examined the effect of atherogenic cytokines (IL-6, TNFα, and Ang II) on EC differentiation and function. MSCs (CD44+, CD73+, CD90+, CD14−, and CD45−) were isolated from the bone marrow of Yucatan microswine. Naïve MSCs cultured in differentiation media containing VEGF-A (50 ng/mL) demonstrated increased expression of EC-specific markers (vWF, PECAM-1, and VE-cadherin), VEGFR-2 and Sox18, and enhanced endothelial tube formation. IL-6 or TNFαcaused a dose-dependent attenuation of EC marker expression in VEGF-A-stimulated MSCs. In contrast, Ang II enhanced EC marker expression in VEGF-A-stimulated MSCs. Addition of Ang II to VEGF-A and IL-6 or TNFαwas sufficient to rescue the EC phenotype. Thus, Ang II promotes but IL-6 and TNFαinhibit VEGF-A-induced differentiation of MSCs into ECs. These findings have important clinical implications for therapies intended to increase cardiac vascularity and reendothelialize coronary arteries following intervention.


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