| Summary: | 碩士 === 國立陽明大學 === 微生物及免疫學研究所 === 100 === In recent years, far infrared radiation therapy (FIR therapy) has been reported to improve hemodynamics, wound recovery and life quality in patients with diabetes, peripheral artery disease or cardiovascular disease. Animal studies demonstrated that FIR therapy increase the recovery of ischemia tissues and endothelial functions. FIR therapy could also increase the efficiency of endothelial progenitor cells (EPCs) release from bone marrow. In our previous studies revealed that FIR therapy elevated the abilities of migration and tube formation in EPCs. In addition, we found FIR therapy could rescue the cell activities in high glucose-treated EPCs. However, the mechanism of how FIR therapy regulate the activities of EPCs is unknown. MicroRNAs have been proven to play an important role in angiogenesis, therefore we used miRNA microarray to analyze the effect of FIR therapy on miRNA expression in EPCs. According to microarray data, we found miR-720 is highly upregulated in EPCs after FIR therapy. Ectopic expression of miR-132 in EPCs in vitro increased their migration and tube-forming capacity, whereas addition of miR-720 inhibitors reduced migration and tube-forming capacity in EPCs. Among the top-ranking predicted targets of miR-720 by using mRNA array and bioinformatics was VASH1, which was a known negative regulator of angiogenesis. We did find that VASH1 is down regulated after FIR therapy in EPCs. Overexpress miR-720 in EPCs, while decreasing the expression of VASH1 and cell migration and tube-forming capacity; however, knockdown miR-720 in EPCs, increasing the expression of VASH1 and cell migration and tube-forming capacity. We concluded that FIR therapy regulate the activities of EPCs by elevating the expression of miR-720 which then repressing the expression of VASH1. Consequently, miR-720 may act as an angiogenic factor in angiogenesis.
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