Research Paper Volume 16, Issue 21 pp 13181—13200

Figure 6. Certain MK CM treatments alter various genes of BMECs to a proangiogenic and proinflammatory phenotype. The changes in mRNA expression were quantified following an overnight incubation period. Data are expressed as a mean ± SD fold change relative to their respective controls with post-hoc p-values listed in each panel (n = 3–4 biological replicates/group). GAPDH was used as an internal control. Significance was determined using one-way ANOVA with Tukey’s post-hoc analysis or Kruskal-Wallis test with Dunn’s post-hoc analysis depending on the normalcy of the data distribution as determined by a Shapiro-Wilk test. MK CM treatments showed trending or significant increases in BMEC expression of CXCR2 (A, B) and PDGFRβ (E, F), while showing trending or significant decreases of CD36 (G, H), CD74 (I, J), and TGFβR2 (K, L) expression. Although aged male and young female MK CM significantly increased CXCR4 expression, young male and aged female MK CM did not (C, D). No significant differences in gene expression levels were seen in BMPR2 (M, N) or CD47 (O, P).