scholarly journals G-CSF and hypoxic conditioning improve the proliferation, neural differentiation and migration of canine bone marrow mesenchymal stem cells

2016 ◽  
Vol 12 (3) ◽  
pp. 1822-1828 ◽  
Author(s):  
Jing Yu ◽  
Xing-Long Liu ◽  
Qi-Guang Cheng ◽  
Shan-Shan Lu ◽  
Xiao-Quan Xu ◽  
...  
2008 ◽  
Vol 22 (4) ◽  
pp. 995-1001 ◽  
Author(s):  
Shabnam Kermani ◽  
Khadijeh Karbalaie ◽  
Seyed Hossein Madani ◽  
Ali Akbar Jahangirnejad ◽  
Mohamadreza Baghaban Eslaminejad ◽  
...  

2022 ◽  
Vol 12 (3) ◽  
pp. 581-587
Author(s):  
Wenxu Rao ◽  
Kang Yin

This study aims at investigating the mechanism underlying bone marrow mesenchymal stem cells (BMSC) function in glioma. Glioma cells were administered with plasmids loading NF-κB siRNA, microRNA (miRNA)-189 inhibitor, or miR-189 mimics for transfection followed by analysis of miR-189 expression by RT-qPCR, cell apoptosis by flow cytometry, cell proliferation by MTT assay,invasion and migration by Transwell assay, inflammatory factors secretion by ELISA as well as proteins expression by western blot. A mouse model of glioma was established to detect the in vivo effect of BMSCs. miR-189 was lowly expressed in glioma cell lines but enriched in BMSCs. When miR-189 was silenced, cell proliferation, invasion and migration were potentiated and apoptosis was decreased, along with enhancement of N-cadherin, Vimentin, MMP-2 and and MMP-9, and decline in Bax, cleaved casepase-3 and cleaved PARP. Silencing of NF-κB reversed the effect of miR-189 inhibitor on cell progression, accompanied with reduction of inflammatory factors. BMSCs treatment effectively promoted miR-189 expression in glioma and inactivated TNF-α/NF-κB signaling, thereby suppressing tumor growth. In conclusion, miR-189 derived from BMSC inhibits glioma progression through regulation of TNF-α/NF-κB signaling pathway.


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