| Gene name: | CGRP |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | NPCs |
| Gene ID: | 796 |
| Category: | protein coding |
| Phenotype: | Intervertebral disc degeneration |
| Experimental category: | L |
| PMID: | 34987701 |
| Experiment: | Safranin O-fast green staining//Immunochemical staining//CCK-8 assay//RT-PCR |
| Description: | To further explore the relationship between CGRP and its receptors, CALCRL and RAMP1, and age, mice with different age of months were further used. As shown in safranin O-fast green staining, the shape of IVD tissue was collapsed in aged mice at 12 months and 18 months compared with 6 months, suggesting the intervertebral disc gradually experienced degeneration with aging. In addition, immunohistochemical analysis revealed the gradually elevated protein expression of CGRP and its receptors, CALCRL and RAMP1, with increasing age in mice. The cell viability of NP cells decreased after being treated by CGRP in a concentration-dependent manner.The mRNA expression of PCNA in human NP cells dose-dependently decreased after being treated with CGRP. |
| Regulatory pathway: | MAPK//NF-κB |
| R-AG-Pathway: | Activation//Activation |
| Official symbol(s): | MAPK//NFKB1 |
| Pathway experiment: | Western blot//Immunofluorescence |
| Pathway description: | Western blot demonstrated that CGRP could dose-dependently enhance the phosphory- lation of MAPK. Besides, NF-κB signaling pathway was also concentration-dependently activated by CGRP, and this activated effect was achieved through the phosphorylation of IκB-α. Immunofluorescence results suggested that the nucleus translocation of p65 was increased when human NP cells were treated with CGRP. |
Annotation:
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