Gene name: | CCL2 |
Aging type: | Accelerate |
Aging characteristic: |
Tissue type: | -- |
Cell name: | UCB-MSC |
Experiment: | SA-β-gal activity assay//Knockdown |
Description: | Compared with the untreated control, MCP-1 treatments significantly increased SA-β-gal activity with passaging by up to 8-fold, concomitantly with a considerable delay in cell growth.The use of siRNA to silence MCP-1 in UCB-MSCs significantly blocked both SA-β-gal activity induction and delayed cell growth . |
Target gene: | CCR2 |
Official symbol(s): | CCR2 |
R-AG-Target gene: | -- |
Subcategory: | Unclear |
Target gene experiment: | Flow cytometry//Western blot//SA-β-gal activity assay//Cell growth kinetics//Colony formation assay |
Target gene description: | MCP-1 is a pro-inflammatory cytokine that exerts its biological effects through its cognate receptor CCR2 (5,45). The expression of CCR2 in UCB-MSCs was lower in the early-phase but it was considerably upregulated in the intermediate-phase and further increased in the terminal senescent phase. Importantly, treatment with CCR2 blocking antibody significantly reduced SA-β-gal expression and enhanced the growth rate and colony-forming capacity of UCB-MSCs in the intermediate-phase. |
Regulatory pathway: | ROS-P38-MAPK-P53-P21 |
R-AG-Pathway: | Activation |
Official symbol(s): | ROS1-MAPK14-MAPK-TP53-CDKN1A |
Pathway experiment: | Western blot//Knockdown |
Pathway description: | MCP-1 treatment activated the p53-p21 signaling cascade, increasing the protein level of p53 phosphorylated at Ser392 and total p21.At the molecular level, MCP-1 KD cells showed attenuated activation of the p53-p21 pathway.Moreover, p38-MAPK, a crucial mediator of ROS-induced senescence, was activated from 8 h and peaked at 18 h after MCP-1 stimulation .Importantly, treatment with SB203580, a chemical inhibitor of p38-MAPK, significantly abrogated the increase in phosphorylated p53 and p21 proteins induced by MCP-1 stimulation. |
Annotation:
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