CXCL12 regulates bone marrow-derived endothelial progenitor cells to promote aortic aneurysm recovery.

Bone marrow-derived endothelial progenitor cells (EPCs) have been proven to participate in the recovery of aortic aneurysm. CXCL12 promotes EPC recruitment and revascularization. Therefore, this study was dedicated to fathoming out whether EPCs regulated by CXCL12 can participate in the recovery of aneurysm. The morphology and maker protein activity of EPCs derived from bone marrow were separately detected by microscopic examination and immunofluorescence. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot were performed to detect the transfection efficiency of CXCL12. Lumen formation, viability, and migration were determined by lumen formation, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), and wound-healing assays, respectively. The aneurysm tissues in rat model of artery aneurysm were used for histopathological observation by haematoxylin-eosin (HE) staining, α-SMA was detected by immunohistochemistry, and the expressions of VEGF, IGF1, FGF, PDGF and matrix metalloproteinase-2/9 (MMP-2/9) were measured by RT-qPCR and western blot assays. As a result, some EPCs showed fusiform on day 6, while others showed a cord-like structure. On day 17, cells presented a paving stone-like pattern. The expressions of CD34, CD133 and VEGFR2 were positive. CXCL12 overexpression promoted lumen formation, viability and migration of EPCs, and further facilitated growth of smooth muscle-like cells in the aneurysm cavity and VEGF expression, while inhibiting MMP-2/9 expression in the aneurysm tissues in vivo. The present study suggested that CXCL12 overexpression strengthened the lumen formation, viability, and migration of EPCs, and CXCL12-primed EPCs had better effects on aneurysm recovery than unmodified EPCs did.