| External factors: | Exosomes |
| Aging type: | Prevent |
| Aging characteristic: |
| Category: | Other |
| Phenotype: | Cardiovascular disease |
| Experiment: | -- |
| Description: | To determine whether exosomes could prevent aginginduced cardiac dysfunction, exosomes were injected into D-gal-treated mice. We found that exosomes attenuated the effects of D-gal in the left ventricular ejection fraction (EF) and fraction shorting (FS), and siMALAT1 blocked the function of exosomes. We also found that exosomes attenuated the effects of D-galactose (D-gal) on telomere length, and the beneficial effects of exosomes were blocked by siMALAT1. |
| Regulatory pathway: | lncRNA MALAT1-NF-κB-TNF-α |
| R-EF-Pathway: | -- |
| Official symbol(s): | MALAT1-NF-κB-TNF |
| Pathway experiment: | Knockdown//SA-β-gal activity assay//Western blot//qRT-PCR |
| Pathway description: | We further demonstrated that exosomes inhibited H2O2-induced NF-κB activity and the expression of NF-κB subunit p-p65 . Exosomes also inhibited H2O2-induced expression of TNF-α at both mRNA and protein levels .Transfection of cardiomyocytes with siMALAT1 led to a reduction in NF-κB activity and the expression level of NF-κB subunit p-p65. siMALAT1 also reduced the expression of TNF-α induced by H2O2 treatment. Moreover, transfection of siMALAT1 inhibited H2O2-induced p21 expression. siMALAT1 blocked the effect of exosomes on β-gal-activity and cell proliferation .These data suggest that exosomes prevent cell senescence through the lncRNA MALAT1/NF-κB/TNF-α pathway. |
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