| Gene name: | AGT |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | HUVEC |
| Gene ID: | 183 |
| Category: | protein coding |
| Phenotype: | Atherosclerosis |
| Experimental category: | L |
| PMID: | 18383564 |
| Experiment: | SA-β-gal activity assay//Flow cytometry//Transmission electron microscopy//Cell morphological analysis |
| Description: | SA-β-gal staining was significantly increased in Ang II-stimulated cells in contrast to the control cells which indicates that Ang II promoted cellular senescence in HUVEC.We found that the cell cycle was at G0-G1, the S phase and G2/M phase tended to disappear in Ang II-induced cells compared with the control cells. Transmission electron microscopy was used to evaluate the ultra-microstructure of HUVEC. Senescent cells appeared flattened and enlarged. Chromatin was condensed at the nuclear margin, invagination of the nuclear membrane and vacuolization of the cytoplasm identified aging cells .But the control cell appeared round and smooth in shape and possessed even chromatin. |
| Target gene: | BCL-2//ERK |
| Official symbol(s): | BCL-2//ERK |
| R-AG-Target gene: | Downregulation//Activation |
| Subcategory: | Unclear |
| Target gene experiment: | Immunocytochemical staining//RT-PCR//Western blot |
| Target gene description: | The decrease in Bcl-2 content during aging.Exposure of cells to 10-6mol L 1 Ang II resulted in activation of ERK as manifested by an increase in ERK phosphorylation. The increased phosphorylation of ERK peaked at 12 h after exposure to Ang II and lasted for 36 h. However, the activity of p-ERK declined to the basal level at 48 h after Ang II treatment. |
| Regulatory pathway: | -- |
| R-AG-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation:
Loading,please wait...