Abstract
Altered microRNA expression is implicated in cardiovascular diseases. Our objective was to determine microRNA signatures in thoracic aortic aneurysms (TAAs) and abdominal aortic aneurysms (AAAs) compared with control non-aneurysmal aortic specimens. We evaluated the expression of fifteen selected microRNA in human TAA and AAA operative specimens compared to controls. We observed significant upregulation of miR-221 and downregulation of miR-1 and -133 in TAA specimens. In contrast, upregulation of miR-146a and downregulation of miR-145 and -331-3p were found only for AAA specimens. Upregulation of miR-126 and -486-5p and downregulation of miR-30c-2*, -155, and -204 were observed in specimens of TAAs and AAAs. The data reveal microRNA expression signatures unique to aneurysm location and common to both thoracic and abdominal pathologies. Thus, changes in miR-1, -29a, -133a, and -221 are involved in TAAs and miR-145, -146, and -331-3p impact AAAs. This work validates prior studies on microRNA expression in aneurysmal diseases.
Highlights
Detection and risk stratification of aortic aneurysms is essential to reduce risk of catastrophic rupture and dissection, which carries high risk of morbidity and mortality [1]
We did not observe any significant age differences between thoracic aortic aneurysms (TAAs) and abdominal aortic aneurysms (AAAs) patient samples, but non-aneurysmal controls were collected from younger patients (Table 1)
Expression of the fifteen miRNAs was analyzed by quantitative reverse transcription polymerase chain reaction (qRT-PCR) in TAA, AAA, and control aortic specimens (Table 2; Figures 1–3)
Summary
Detection and risk stratification of aortic aneurysms is essential to reduce risk of catastrophic rupture and dissection, which carries high risk of morbidity and mortality [1]. Aortic aneurysms occur secondary to pathologic remodeling of the aortic wall and are frequently associated with hypertension [2], atherosclerosis [3,4] in the abdominal aorta, and bicuspid aortopathy [5], or connective tissue disorders [6] in the ascending thoracic aorta. Ascending thoracic aortic aneurysms (TAAs) frequently result from a non-inflammatory process of cystic medial degeneration including smooth muscle cell (SMC) loss and elastin fragmentation [7]. Descending TAAs and abdominal aortic aneurysms (AAAs) involve elastic degeneration, but this can occur via an inflammatory and atherosclerotic process. Identification of biomarkers that are driven by aortic remodeling is important to allow for early identification and risk stratification. Biomarkers may represent therapeutic targets to prevent aneurysm expansion
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