Fig. 7

ha-MSCs exposed to inflammatory conditions assume a pathological phenotype. a PBMCs isolated from AAA patients showed a molecular signature reporting high levels of inflammatory cytokines (TNF-α and IL-1β) and reduced anti-inflammatory IL-10. Results are expressed as fold changes relative to healthy PBMCs. b According to the experimental design, ha-MSCs were exposed to inflammatory mediators (cytokines and PBMCs) for 24 hours, then investigated in terms of vascular remodelling and differentiation properties. ha-MSCs exposed to inflammation underwent increased transcription of (c) MMP-9 and (d) osteogenic lineage-specific markers (BMP-2, OPN, OCN), to the detriment of the adipogenic transcriptional factor PPAR-γ. Results are expressed as fold changes relative to unexposed ha-MSCs. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. e Western blot analysis of MMP-9 was performed on serum-free conditioned media, whereas PPAR-γ, BMP-2 and OPN were detected in cell lysates. PBMC peripheral blood mononuclear cell, TNF-α tumour necrosis factor alpha, IL interleukin, ha-PMSC healthy aortic PMSC, AAA-PMSC abdominal aortic aneurysm PMSC, MSC mesenchymal stem cell, MMP-9 matrix metalloproteinase-9, BMP-2 bone morphogenetic protein-2, OPN osteopontin, OCN osteocalcin, PPAR-γ peroxisome proliferation activated receptor gamma, ctrl control