Aortic α-smooth muscle actin expressions in aortic disorders and coronary artery disease: An immunohistochemical study

نویسندگان

  • Shi-Min Yuan
  • Ning Wu
چکیده

OBJECTIVE The is to report immunohistochemical observations of aortic α-smooth muscle actin (SMA) expressions in patients with aortic aneurysm, acute aortic dissection, and coronary artery disease and to discuss phenotypic switching of smooth muscle cells (SMCs) of these lesions. METHODS Forty-nine consecutive patients scheduled for surgical treatment for acute type A aortic dissection (20 patients), aortic aneurysm (9 patients), and coronary artery disease (20 patients) were included. Surgical specimens of the aorta were obtained and prepared for hematoxylin and eosin and immunohistochemical stainings. RESULTS A comparison of aortic structural changes between the three groups showed that patients with coronary artery disease had the least severe aorta degeneration with the most intense α-SMA positivity. Aortic structural impairment was the most severe in patients with aortic dissection, whereas α-SMA positivity was more intense in patients with aortic dissection than in those with aortic aneurysm. CONCLUSION Disparities in α-SMA expressions in the aortic tissues of the three groups represent the extent of SMC degenerations or a phenotypic switching between contractile and synthetic SMCs. The results imply severe SMC degenerations in patients with aortic aneurysm, which may be beneficial because of the production of extracellular matrix necessary for healing of the vascular wall, but severe disruptions in elastic fibers in patients with aortic dissection. Patients with coronary artery disease show slight SMC degeneration and phenotypic switching among the three groups. The possible apoptotic and genetic mechanisms of aortic structural impairments warrant further elaborations.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

α-Smooth Muscle Actin and ACTA2 Gene Expressions in Vasculopathies

α-smooth muscle actin, encoded by ACTA2 gene, is an isoform of the vascular smooth muscle actins, typically expressed in the vascular smooth muscle cells contributing to vascular motility and contraction. ACTA2 gene mutations cause a diversity of diffuse vasculopathies such as thoracic aortic aneurysms and dissections as well as occlusive vascular diseases, including premature coronary artery d...

متن کامل

Correlation Between Aortic Valve Sclerosis and Coronary Artery Disease: A Cross - Sectional Study

  Introduction: Aortic valve sclerosisis considered as a manifestation of coronary atherosclerosis. Recent studies demonstrated an association between aortic valve sclerosis and obstructive coronary artery disease. The purpose of this study was to evaluatethe correlation betweenaortic valve sclerosis andobstructive coronary artery disease and the extent of coronary artery disease in patients ho...

متن کامل

Neopterin Counters Vascular Inflammation and Atherosclerosis

BACKGROUND Neopterin, a metabolite of GTP, is produced by activated macrophages and is abundantly expressed within atherosclerotic lesions in human aorta and carotid and coronary arteries. We aimed to clarify the influence of neopterin on both vascular inflammation and atherosclerosis, as neither effect had been fully assessed. METHODS AND RESULTS We investigated neopterin expression in coron...

متن کامل

Vascular disease-causing mutation, smooth muscle α-actin R258C, dominantly suppresses functions of α-actin in human patient fibroblasts.

The most common genetic alterations for familial thoracic aortic aneurysms and dissections (TAAD) are missense mutations in vascular smooth muscle (SM) α-actin encoded by ACTA2 We focus here on ACTA2-R258C, a recurrent mutation associated with early onset of TAAD and occlusive moyamoya-like cerebrovascular disease. Recent biochemical results with SM α-actin-R258C predicted that this variant wil...

متن کامل

Mutations in smooth muscle alpha-actin (ACTA2) cause coronary artery disease, stroke, and Moyamoya disease, along with thoracic aortic disease.

The vascular smooth muscle cell (SMC)-specific isoform of alpha-actin (ACTA2) is a major component of the contractile apparatus in SMCs located throughout the arterial system. Heterozygous ACTA2 mutations cause familial thoracic aortic aneurysms and dissections (TAAD), but only half of mutation carriers have aortic disease. Linkage analysis and association studies of individuals in 20 families ...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره 19  شماره 

صفحات  -

تاریخ انتشار 2018