RESUMEN
BACKGROUND: Preliminary study has shown that overexpression of GATA-4-overexpressing bone marrow mesenchymal stem cell (BMSCs) exosomes (BMSCsGATA-4-exosome) can promote BMSCs differentiate into cardiomyocytes, indicating it can repair myocardial infarction. Additionally, high expression of miRNA-673-5p is observed in miRNA-673-5p BMSCsGATA-4-exosome and focal myocardium of myocardial infarction, which involve in cell differentiation, suggesting that miRNA-673-5p may be a key molecular of BMSCsGATA-4-exosome for repairing myocardial infarction. OBJECTIVE: To investigate the molecular regulatory network of BMSCsGATA-4-exosomes that promotes BMSCs differentiation into cardiomyocyte-like cells. METHODS: miR-673-5p-mimic was added to the BMSCs culture system as an experimental group (BMSCsmiR-330-3p-mimic ). BMSCsGATA-4, BMSCsGATA-4-empty vector, BMSCs and BMSCsGATA-4-miR-673-5p-inhibitor groups were set as confounding factor control groups. The exosomes and myocardial cells secreted by each group were co-cultured for 24 hours. The expression levels of myocardium specific molecules α-actin, Desmin, cTnT and Cx43 were detected by immunofluorescence and RT-PCR. The expression levels of the corresponding miRNA-673-5p target genes TSC-1, ERK1/2 and Mef2c were detected through western blot assay based on the prediction results of the microRNA target gene. RESULTS AND CONCLUSION: The BMSCsmiR-673-5p-mimic-exosome+BMSCs culture group had the highest α-actin, Desmin, cTnT and Cx43 levels (P < 0.05), and the lowest TSC-1 expression (P < 0.05). In summary, BMSCsGATA-4-exosome inhibits the expression of TSC-1 via miRNA-673-5p to promote BMSCs differentiation into cardiomyocyte-like cells.
RESUMEN
Abstract Aortopulmonary septal defect, also known as the aortopulmonary window, is a rare congenital macrovascular malformation. This case involves a 9-year-old boy with aortopulmonary septal defect (type I combined with type IV). Before surgery, milrinone and alprostadil were used to counteract high lung pressure. Surgery was performed under cardiopulmonary bypass, following which the pulmonary pressure decreased. The aorta was cut, and the right pulmonary artery opening was connected with the main pulmonary artery septal defect using polyester patch. An internal tunnel was made, and the deformity correction was completed. The child exhibited normal postoperative recovery with no discomfort. A complex aortopulmonary window is a rare condition that can be treated successfully with appropriate preoperative and surgical management.