Fig. 6 | npj Aging and Mechanisms of Disease

Fig. 6

From: Clampdown of inflammation in aging and anticancer therapies by limiting upregulation and activation of GPCR, CXCR4

Fig. 6

Role of CXCR4 receptor and its upregulation in DNA-damage associated inflammation. a Effect of CXCR4 receptor level changes on enhanced inflammation during DNA damage. IL8 levels measured from HeLa cells where expression of CXCR4 (left) or HIF1α (right) was knocked down using gene specific shRNAs. Experiments were performed as described in Fig. 5a. b Analysis of inflammatory response in CXCR4-OE cells. CXCR4-GFP cells were treated with BrdU or BrdU + CXCL12 and IL8 ELISA was performed. c Analysis of gene expression changes during organismal aging. Quantitative RT-PCR analysis for the expression of p21, IL8 and CXCR4 in liver tissues of 2-months and 18-months old BALB/c mice. The values were normalized to GAPDH expression levels. d Analysis of gene expression changes during IR mediated damage in C57BL/6 mice. Quantitative RT-PCR analysis for the expression of p21 and CXCR4 in irradiated animals. e Analysis of IL8 levels during irradiation and in response to various inhibitors. Animals were treated with Caffeine (Caff), Plerixafor (Plx) or Rolipram (Roli) alone or with these compounds and irradiation. Gene expression changes for IL8 was tested in liver as mentioned in Fig. 6c. For all experiment, n > 5 and as indicated in the figure panels. p-value or significance was determined by ANOVA and Bonferroni’s multiple comparison test. Significance (p value) is represented as *, *≤0.05, **≤0.01, ***≤0.001, and ****≤0.001 and ns, where >0.05 for “not significant”