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Background: Adipose-derived stem cells (ASCs) hold a great promise for myocardial infarction, but therapeutic efficacy appears to be limited by their poor survival and engraftment. Integrins are transmembrane proteins known to regulate the biological behaviors of stem cells. Integrin β 2 (ITGB2) specifically binds to intercellular cell adhesion molecule-1 (ICAM-1), which is upregulated in infarcted myocardium. ASCs typically express an insufficient amount of ITGB2, and this may limit their homing and engraftment abilities.Methods: ASCs were lentivirally transduced to overexpress ITGB2. ITGB2 messenger RNA (mRNA) and protein expression were examined by quantitative polymerase chain reaction (PCR) and western blot. Cell viability, proliferation, and migration were assessed in vitro. Adipogenic and osteogenic differentiation were induced, and the mRNA expressions of specific differentiation markers were quantified by PCR. ICAM-1 expression in the infarcted myocardium was quantified at 3 and 7 days after myocardial infarction. ITGB2transfected ASCs (ITGB2-ASCs), control ASCs (CTRL-ASCs), and phosphate-buffered saline (PBS) were intramyocardially injected into the peri-infarct region at 3 days after coronary ligation. Four weeks after transplantation, myocardial blood perfusion was measured by 13 N•NH 3 •H 2 O 2 positron emission tomography (PET)/computed tomography (CT). Explanted hearts were then processed for the measurement of capillary density, the quantification of survived green fluorescent protein (GFP + ) ASCs, and the identification of ASCs coexpressing angiogenic growth factors.Results: ICAM-1 expression peaked at 3 days after myocardial infarction and remained elevated over the remote normal myocardium at 7 days after myocardial infarction. ITGB2-ASCs displayed a significant increase in cell viability, proliferation rate, and migration index when compared with CTRL-ASCs.Adipogenic and osteogenic differentiation were more enhanced in ITGB2-ASCs than in CTRL-ASCs. Four weeks after transplantation, surviving GFP + ASCs were significantly increased, ASCs expressing angiogenic growth factors were more pronounced, capillary density was substantially enlarged, and myocardial blood perfusion was markedly improved in the hearts that received ITGB2-ASCs implantation when compared to those that underwent CTRL-ASC treatment.Conclusions: ITGB2 overexpression of ASCs enhanced cell viability, proliferation, and migration and induced differentiation in vitro. ITGB2 overexpression significantly improved the survival and engraftment of ASCs into infarcted myocardium via ITGB2/ICAM-1 interaction, augmented angiogenesis, and ultimately improved blood perfusion in infarcted myocardium.

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Background: Thoracic endovascular aortic repair (TEVAR) for type B aortic dissection (TBAD) induces false lumen (FL) thrombosis, promotes favorable aortic remodeling, and makes an impact on abdominal aortic branch perfusion patterns. However, little is known about the long-term fate of aortic remodeling and abdominal aortic branch perfusion after TEVAR for TBAD and the effect of FL thrombosis status on these changes.Materials and methods: Between January 2014 and May 2021, 59 enrolled patients with acute TBAD were treated with TEVAR and had post-operative or follow-up images. Pre-operative, post-operative, and latest follow-up CT angiography (CTA) data were analyzed for the largest diameter of true lumen (TL), FL, and transaorta and for the FL thrombosis status on the stented thoracic aorta, unstented thoracic aorta, and abdominal aorta. Abdominal aorta perfusion patterns were characterized.Results: The mean follow-up period was 17.1 months. In the stented thoracic aorta, average TL diameters increased, average FL diameters decreased, and average transaortic diameters did not change; 82.6% of the patients had either a stable or shrinking transaortic size and 87% of the patients achieved total FL thrombosis. In the unstented thoracic aorta, average TL diameters increased, transaortic growth and no changes occurred in 39.1 and 45.7% of the patients, respectively, and complete FL thrombosis was present in 50% of the patients. In the abdominal aorta, average FL and transaortic diameters increased, aorta was expanded in 52.2% of the patients, and FL remained patent in 65.2% of the patients. Of the 354 branches, 37 branches (10.5%) exhibited changes in perfusion patterns, 22 branches (6.2%) demonstrated an increased TL perfusion, and 15 branches (4.2%) had an increased FL contribution. Compared with patent or partially thrombosed FL, complete FL thrombosis was accompanied by a bigger decrease in FL diameters, a larger increase in TL diameters, and a higher percentage of abdominal branch TL perfusion.Conclusions: In majority of the patients, TEVAR stabilized the size of the stented thoracic aorta, namely TL expansion and FL obliteration. However, abdominal aortic FL remained patent FL, and it was expanded with the resultant transaortic growth over a long follow-up period. Abdominal aortic branch perfusion patterns remained largely stable after TEVAR. The failure to achieve FL thrombosis negatively affects the remodeling of a contagious abdominal aortic dissection.