Human Umbilical Cord-Derived Mesenchymal Stem Cells Relieve Hind Limb Ischemia by Promoting Angiogenesis in Mice

2019 ◽  
Vol 28 (20) ◽  
pp. 1384-1397 ◽  
Author(s):  
Zhecun Wang ◽  
Liang Zheng ◽  
Chong Lian ◽  
Yunling Qi ◽  
Wen Li ◽  
...  



2021 ◽  
Author(s):  
Hideaki Yamada ◽  
Naoaki Sakata ◽  
Masuhiro Nishimura ◽  
Tomoko Tanaka ◽  
Masayuki Shimizu ◽  
...  




Stem Cells ◽  
2008 ◽  
Vol 26 (10) ◽  
pp. 2625-2633 ◽  
Author(s):  
Shin Ishikane ◽  
Shunsuke Ohnishi ◽  
Kenichi Yamahara ◽  
Masaharu Sada ◽  
Kazuhiko Harada ◽  
...  


2019 ◽  
Vol 56 (2) ◽  
pp. 77-91
Author(s):  
María-Dolores García-Vázquez ◽  
Borja Herrero de la Parte ◽  
Ignacio García-Alonso ◽  
María-Celia Morales


2017 ◽  
Vol 117 (10) ◽  
pp. 1908-1918 ◽  
Author(s):  
Elisa Rossi ◽  
Céline Goyard ◽  
Audrey Cras ◽  
Blandine Dizier ◽  
Nour Bacha ◽  
...  

SummaryEndothelial colony-forming cells (ECFCs) are progenitor cells committed to endothelial lineages and have robust vasculogenic properties. Mesenchymal stem cells (MSCs) have been described to support ECFC-mediated angiogenic processes in various matrices. However, MSC-ECFC interactions in hind limb ischemia (HLI) are largely unknown. Here we examined whether co-administration of ECFCs and MSCs bolsters vasculogenic activity in nude mice with HLI. In addition, as we have previously shown that endoglin is a key adhesion molecule, we evaluated its involvement in ECFC/MSC interaction. Foot perfusion increased on day 7 after ECFC injection and was even better at 14 days. Co-administration of MSCs significantly increased vessel density and foot perfusion on day 7 but the differences were no longer significant at day 14. Analysis of mouse and human CD31, and in situ hybridization of the human ALU sequence, showed enhanced capillary density in ECFC+MSC mice. When ECFCs were silenced for endoglin, coinjection with MSCs led to lower vessel density and foot perfusion at both 7 and 14 days (p<0.001). Endoglin silencing in ECFCs did not affect MSC differentiation into perivascular cells or other mesenchymal lineages. Endoglin silencing markedly inhibited ECFC adhesion to MSCs. Thus, MSCs, when combined with ECFCs, accelerate muscle recovery in a mouse model of hind limb ischemia, through an endoglindependent mechanism.Supplementary Material to this article is available online at www.thrombosis-online.com.



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