| Gene name: | MIR194-1 |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | HUVEC |
| Experiment: | qRT-PCR//SA-β-gal activity assay//Western blot//DAPI staining//BrdU assay |
| Description: | The increase of miR-194 expression in replicative senescence was validated in human umbilical vein epithelial cells (HUVECs) as well. In order to further confirm the function of miR-194 on cellular senescence, we transfected MEFs with miR-194 inhibitor, Antagomir 194 or Antagomir NC. The results unveiled that miR-194 inhibition by Antagomir 194 transfection conferred attenuated senescence phenotype and enhanced proliferation of MEFs. Consistently, the data of SA-β-gal staining and BrdU assay showed that increased expression of miR-194 conferred NIH/3T3 cells with enhanced H2O2-induced senescence and diminished cell proliferation. In contrast, inhibition of miR-194 protected NIH/3T3 cells against H2O2 induced senescence. |
| Target gene: | DNMT3A |
| Official symbol(s): | DNMT3A |
| R-AG-Target gene: | Downregulation |
| Subcategory: | Unclear |
| Target gene experiment: | Dual-Luciferase reporter assay//Western blot |
| Target gene description: | We further constructed a luciferase reporter vector carrying mutant fragment of DNMT3A-3’UTR-2. The results showed that mutation of the miR-194 binding site in the DNMT3A 3’UTR (mut-DNMT3A-2) significantly reversed the Agomir 194-dependent reduction of luciferase reporter activity.Subsequently, we examined the DNMT3A mRNA and protein expression levels in MEFs after transfection with Agomir NC or Agomir 194. The data showed that Agomir 194 transfection significantly suppressed the expression of endogenous DNMT3A at both mRNA and protein levels. |
| Regulatory pathway: | -- |
| R-AG-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation:
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