Potential function of microRNAs in thoracic aortic aneurysm and thoracic aortic dissection pathogenesis

Abstract

Thoracic aortic aneurysm (TAA) and thoracic aortic dissection (TAD) are aortic diseases known as 'silent killers'. While TAA is characterized by an enlargement of at least half of the normal aortic diameter, TAD is characterized by progressive pseudo‑lumen formation, which results in the gradual separation of the aortic wall layers. In the present study, a total of 28 serum samples from nine patients with TAA, nine patients with TAD and ten healthy individuals were studied. The aim of the present study was to investigate the expression profiles of hsa‑microRNA(miR)‑143‑3p and hsa‑miR‑22‑3p in TAA and TAD in order to identify candidate miRNAs that are responsible for the pathogenesis of the diseases. Following the detection of target mRNAs from candidate miRNAs by bioinformatic tools, the expression profiles of target mRNAs were analyzed. A quantitative polymerase chain reaction was performed to detect Kirsten rat sarcoma viral oncogene homolog (KRAS), mitogen‑activated protein kinase (MAPK) 7, MAPK14 and transgelin (TAGLN) mRNA expression profiles. The results of the comparison with control group demonstrated that the increase in the expression levels of hsa‑miR‑143‑3p (P=0.017) and hsa‑miR‑22 (P=0.03) candidate miRNAs were statistically significant in the TAA group, but not in the TAD group. The expression of KRAS and MAPK7 mRNAs decreased in the two groups compared with the control group. The level of expression of MAPK14 decreased in the TAD group, but increased in the TAA group compared with the control group. TAGLN mRNA expression level increased in the two groups. The statistically significant difference in the expression of hsa‑miR‑143‑3p suggests that hsa‑miR‑143‑3p may be a potential biomarker for TAA, as the expression of the target mRNAs KRAS and MAPK7 decreased and the miRNA‑mRNA association was negatively correlated. These miRNAs and their associated genes may serve important functions in TAA formation, the altered expression of which may be important in the pathogenesis of TAA.