====== miR 29c ======

Using a quantitative [[miR 29c]] reporter, Bier et al., demonstrated that the PL-[[MSC]] effects were partly mediated by the transfer of exosomal miR-29c. Intramuscular transplantation of PL-MSCs in mdx mice resulted in decreased creatine kinase levels. PL-MSCs significantly decreased the expression of [[TGF]]-β and the level of [[fibrosis]] in the diaphragm and cardiac muscles, inhibited inflammation and increased utrophin expression. In vivo imaging analyses using MSCs labeled with gold [[nanoparticle]]s or fluorescent dyes demonstrated localization of the cells in the muscle tissues up to 3 weeks post treatment. Altogether, these results demonstrate that PL-MSCs and their secreted exosomes have important clinical applications in cell therapy of DMD partly via the targeted delivery of exosomal miR-29c
((Bier A, Berenstein P, Kronfeld N, Morgoulis D, Ziv-Av A, Goldstein H,
Kazimirsky G, Cazacu S, Meir R, Popovtzer R, Dori A, Brodie C. Placenta-derived
mesenchymal stromal cells and their exosomes exert therapeutic effects in
Duchenne muscular dystrophy. Biomaterials. 2018 May 3;174:67-78. doi:
10.1016/j.biomaterials.2018.04.055. [Epub ahead of print] PubMed PMID: 29783118.)).

MiR-29c [[overexpression]] increased [[TMZ]] efficacy in cultured [[glioma cell]]s and in mouse xenograft models. The miR-29c levels were positively correlated with patient outcomes. Our data suggest miR-29c may be potential therapeutic targets for glioma treatment
((Xiao S, Yang Z, Qiu X, Lv R, Liu J, Wu M, Liao Y, Liu Q. miR-29c contribute to
glioma cells temozolomide sensitivity by targeting O6-methylguanine-DNA
methyltransferases indirectely. Oncotarget. 2016 Jul 1. doi:
10.18632/oncotarget.10357. [Epub ahead of print] PubMed PMID: 27384876.
)).