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. Author manuscript; available in PMC: 2021 Dec 8.
Published in final edited form as: Nat Aging. 2021 Jul 12;1:598–615. doi: 10.1038/s43587-021-00082-y

Fig. 6 |. CXCL9 promotes a vascular stiffness gene expression signature in the aging endothelium and impairs endothelial function.

Fig. 6 |

The expression levels of hallmark vascular stiffness genes—CAMs, MMPs and COLs—were analyzed in Scramble and CXCL9-KD aging cells. a, CAMs, MMPs and COLs are highly expressed in Scramble passage 8 compared to passage 0. b, Knockdown of CXCL9 completely restores the expression of CAMs and MMPs, but not COLs. c, Line graph of percent relaxation of mouse thoracic aortic sections incubated with increasing concentrations of CXCL9 shows impaired vascular reactivity to acetylcholine, suggesting that CXCL9 dampens vascular function. d, A similar trend is observed when CXCL9 is given to either young or old mice. CXCL9 disrupts the relaxation supposedly induced by acetylcholine. All data are represented as mean ± s.e.m., n = 3, *Padj value of young mice (PBS) versus young mice (CXCL9) = 0.0237; #Padj value of young mice (PBS) versus old mice (PBS) = 0.0003, $Padj value of young mice (PBS) versus young mice (CXCL9) < 0.0001. Statistical analyses were performed using two-way ANOVA followed by a Bonferroni post hoc test; n = 3 (three separate segments of aortas).