| Gene name: | H19 |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | HUVEC |
| Gene ID: | 283120 |
| Category: | ncRNA |
| Phenotype: | Cardiovascular disease |
| Experimental category: | HL |
| PMID: | 30107531 |
| Experiment: | SA-β-gal activity assay//Western blot//Flow cytometry//Knockdown |
| Description: | We first analyzed the role of H19 in proliferation. siRNA-mediated depletion of H19 in HUVECs led to a significant reduction of cells in S- and G2/M-phase, while cells accumulated in G0/G1 phase;silencing of H19 increased the number of acidic β-galactosidase positive HUVECs and hCoAECs, which is a marker of cellular senescence;Lentivirus-mediated overexpression of H19 tended to reduce p16 and p21 expression;These findings demonstrate that H19 negatively regulates the well-described increase in inflammatory activation in aging. |
| Regulatory pathway: | STAT3 |
| R-AG-Pathway: | Downregulation |
| Official symbol(s): | STAT3 |
| Pathway experiment: | qRT-PCR |
| Pathway description: | STAT3 is known to regulate p21 and ICAM-1,the inhibition of STAT3 with Cryptotanshinone (CPT) abolished the H19 depletion-mediated induction of p21. Furthermore, the induction of ICAM-1 and VCAM-1 after H19 depletion was attenuated by STAT3 inhibition as well . |
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