Review
Copyright ©The Author(s) 2015.
World J Cardiol. Nov 26, 2015; 7(11): 707-718
Published online Nov 26, 2015. doi: 10.4330/wjc.v7.i11.707
Figure 1
Figure 1 Toll-like receptor 3-mesenchymal stem cells enhance to secrete paracrine factors. RNA mimetic polyinosinic-polycytidylic acid [poly(I:C)] stimulated TLR3 system on MSCs. TLR3-MSCs secreted a variety of paracrine factors. RT-PCR detected significant upregulation of SDF1, VEGF and IL6 while inflammation related cytokines (IL-1α, TNFα) were downregulated. Injection of TLR3-MSCs in cardiomyopathy model improved cardiac function more than standard MSCs in association with increasing myocyte proliferation, reducing fibrosis and myocyte apoptosis. TLR3: Toll-like receptor 3; MSCs: Mesenchymal stem cells; SDF1: Stromal cell-derived factor-1; VEGF: Vascular endothelial growth factor; IL: Interleukin; TNF: Tumor necrosis factor.
Figure 2
Figure 2 The effect of cardiosphere-derived cells on myocyte cell size and MAP kinase in the dysfunctional left anterior descending vs remote regions. A: Images (PAS staining) demonstrate that hypertrophied myocytes in untreated hibernating LAD became smaller after CDCs. Myofibrils were condensed indicating the production of healthy myocytes; B: Myocyte diameter was significantly reduced in hibernating LAD and remote regions; C: Corresponding to the morphological change, protein level of MAP3K was downregulated in LAD and remote regions. Data indicates CDCs induced myocyte regeneration and hypertrophy regression. CDCs: Cardiosphere-derived cells; LAD: Left anterior descending; RCA: Right coronary artery.