| Gene name: | NEAT1 |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | BM-MSC |
| Experiment: | SA-β-gal activity assay//qRT-PCR |
| Description: | QRT-PCR results suggested that exosomeMIF transferred LncRNA–NEAT1 to cardiomyocytes, while silencing LncRNA–NEAT1 in MSCs blocked the transfer process. In the subsequent experiments, exosomeMIF significantly reduced the percentage of cells in the G0/G1 phase, expression of p27 and p16, and number of SA-β-gal-positive cells. However, it elevated the telomere length and activity. |
| Target gene: | MIR-221-3P |
| Official symbol(s): | MIR-221-3P |
| R-AG-Target gene: | Inhibition |
| Subcategory: | Unclear |
| Target gene experiment: | Dual-Luciferase reporter assay//qRT-PCR//SA-β-gal activity assay |
| Target gene description: | LncRNA–NEAT1 contains the binding site for miR-221-3p, suggesting that lncRNA as a ceRNA sponged miR-221-3p to limit its function, which was confirmed by dual-luciferase gene reporter assay. As illustrated in Fig. 6b, the co-transfection of miR-221-3p significantly inhibited the luciferase activities elicited by LncRNA–NEAT1. Further, a biotin–avidin pulldown system was employed to test whether miR-221-3p could pull down NEAT1. Cardiomyocytes were transfected with biotinylated miR-221-3p, then collected for biotin based pulldown assay. NEAT1 was pulled down as analyzed by qRT-PCR. Further, a biotin–avidin pulldown system was employed to test whether miR-221-3p could pull down NEAT1. Cardiomyocytes were transfected with biotinylated miR-221-3p, then collected for biotin based pulldown assay. NEAT1 was pulled down as analyzed by qRT-PCR. Importantly, miR-221-3p overexpression markedly increased the number of cells in the G0/G1 phase, expression of p27 and p16, and number of SA-β-gal-positive cells, but inhibited the telomere and telomerase activity, even when exosomeMIF were added to Dox-treated cardiomyocytes. |
| Regulatory pathway: | -- |
| R-AG-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation:
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