| Gene name: | BMP5 |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | Chondrocytes |
| Gene ID: | 653 |
| Category: | protein coding |
| Phenotype: | Osteoarthritis |
| Experimental category: | L |
| PMID: | 33744859 |
| Experiment: | SA-β-gal activity assay//qRT-PCR//Western blot |
| Description: | We then performed SA-β-gal staining assay to determine the role of BMP5 in OA-related chondrocyte senescence. IL-1β-treated BMP5 knockdown chondro- cytes showed significantly lower SA-β-gal activity than the corresponding controls. Western blotting analysis showed that p16, p21, HMGB1, and p53 protein levels were significantly reduced in the IL-1β-treated BMP5- silenced chondrocytes compared to the corresponding controls. Next, we analyzed γH2AX staining to determine if BMP5 knockdown reduced premature senescence of the chondrocytes. We observed that the relative area of γH2AX staining was significantly lower in the IL-1β- treated BMP5-depleted chondrocytes compared to the IL-1β-treated control chondrocytes. We also demonstrated that p16 and p21 protein levels were significantly lower in the knee joint cartilage tissues from the DMM+LV-siBMP5 group mice compared to those from the DDM+LV-siNC group mice. |
| Regulatory pathway: | P38-ERK |
| R-AG-Pathway: | Activation |
| Pathway experiment: | Western blot |
| Pathway description: | We analyzed the status of the p38/ERK signaling pathway in control and BMP5-silenced chondrocytes subjected to IL-1β treatment by western blotting. The levels of total and phosphorylated p38 and ERK1/2 proteins were significantly higher in the IL-1β- treated control chondrocytes compared to the IL-1β treated BMP5-silenced chondrocytes. Moreover, the levels of p38 and ERK1/2 proteins were significantly increased in a dose-dependent manner by incubating chondrocytes with recombinant BMP5. |
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