Expression of Lumican in Thickened Intima and Smooth Muscle Cells in Human Coronary Atherosclerosis

2002 ◽  
Vol 72 (2) ◽  
pp. 142-149 ◽  
Author(s):  
Munehiko Onda ◽  
Toshiyuki Ishiwata ◽  
Kiyoko Kawahara ◽  
Ruojiao Wang ◽  
Zenya Naito ◽  
...  
Life Sciences ◽  
2001 ◽  
Vol 68 (8) ◽  
pp. 933-942 ◽  
Author(s):  
Yukihiro Chino ◽  
Toshiya Minagawa ◽  
Yoshiro Kohno ◽  
Yoshihisa Toda ◽  
Shigeru Murakami ◽  
...  

Circulation ◽  
2015 ◽  
Vol 131 (suppl_2) ◽  
Author(s):  
Kenji Hamaoka ◽  
Maiko Fujii ◽  
Yuki Kuchitsu ◽  
Ayako Yoshioka ◽  
Akiko Okamoto ◽  
...  

Background: Atherosclerotic coronary heart disease has recently emerged as a clinical issue among young individuals with a history of Kawasaki disease (KD), which is a systemic vasculitis unique to children. However, whether or not and how KD promotes atherosclerosis remains unclear. We hypothesized that, analogous to the pathogenesis of arteriosclerosis or atherosclerosis, endothelial injury and the resultant intimal thickening are induced in coronary arteries after attenuation of vasculitis. Methods: We used a rabbit model of KD developed by Onouchi et al. and performed histopathological analysis of the coronary arteries at acute (1, 3, 5, and 7 days) and chronic (3 months) phases of the disease. Results: In these rabbit models, a pan-arteritis with significant intimal cellular hypertrophy was histologically detected in the acute phase, and arterial intimal thickening was observed during the chronic phase. Immunohistochemical analysis of the coronary arteries revealed that the thickened intimal lesions observed during the chronic phase comprised abundant α-smooth muscle actin (α-SMA)-positive cells, most of which concomitantly expressed vascular cell adhesion molecule-1 and nuclear factor-κB. Although macrophages positive for RAM11 were barely detected, macrophage colony stimulating factor was strongly expressed in migrating smooth muscle cells in the intimal layer. In addition, the accumulation of proteoglycan as extracellular matrix was distinctly visible in the thickened intima, indicating progressive accumulation of lipids and proliferation of smooth muscle cells within the lesion. Conclusions: These findings suggest that, in KD-associated vasculitis, the migration of α-SMA-positive cells into the thickened intima might induce continuous vascular inflammation and remodeling, which might progress to coronary arteriosclerosis or atherosclerosis.


2006 ◽  
Vol 134 (Suppl. 1) ◽  
pp. 9-16
Author(s):  
Vesna Lackovic ◽  
Irena Vukovic

INTRODUCTION. Vascular remodelling is an adaptive process involving the adjustment of the structure and function of blood vessels to long-term changes in haemodynamic conditions. This process leads to structural alterations within vessel walls in different cardiovascular diseases, such as hypertension, atherosclerosis, and coarctation of the aorta. OBJECTIVE. We investigated the histochemical and immunocytochemical characteristics of morphological lesions in coronary atherosclerosis and coarctation of the aorta. METHOD. Twenty-one samples of atherosclerotically modified right coronary arteries, divided into 6 segments, were analysed. We also examined 10 samples of coarctation segments, excised during surgery. The segments were stained histochemically (using orcein and alcian blue-PAS), immunocytochemically (using ?-smooth muscle actin-?-SMA, vimentin, desmin, myosin heavy chains-MHC, CD3, CD45, S-100, and Proliferating Cell Nuclear Antigen-PCNA), and for electron microscopy. RESULTS. The results of our study of morphological lesions in coronary atherosclerosis demonstrated initial functional and then, in the later stages of atherosclerosis, morphological, damage to the endothelium. The preatheroma stage revealed the presence of intimal dedifferentiation of smooth muscle cells, with the expression of vimentin and ?-SMA, and the lack of expression of desmin. Along with these changes, a huge number of foam cells of variant origin were noticed. Some of them were CD68-immunoreactive while others were both vimentin- and S-100-immunoreactive. All examined samples of the coarctation of the aorta demonstrated the presence of dedifferentiated smooth muscle cells as well as a diminution in cell numbers, followed by apoptotic smooth muscle cells, and the absence of inflammatory cells. CONCLUSION. Some foam cells develop from monocytemacrophage lineage (CD68-immunoreactive), while others originate from smooth muscle cells (vimentin and S-100- immunoreactive). Coarctation of the aorta is characterised by a diminution in cell numbers (apoptosis) as well as their dedifferentiation from contractile to synthetic phenotype.


2011 ◽  
Vol 4 (02) ◽  
pp. 69-73 ◽  
Author(s):  
Kimikazu Hamano ◽  
Hiroshi Ito ◽  
Kouichi Ueki ◽  
Yoshihiko Fujimura ◽  
Hidetoshi Tsuboi ◽  
...  

2003 ◽  
Vol 100 (8) ◽  
pp. 4754-4759 ◽  
Author(s):  
N. M. Caplice ◽  
T. J. Bunch ◽  
P. G. Stalboerger ◽  
S. Wang ◽  
D. Simper ◽  
...  

Author(s):  
J.M. Minda ◽  
E. Dessy ◽  
G. G. Pietra

Pulmonary lymphangiomyomatosis (PLAM) is a rare disease occurring exclusively in women of reproductive age. It involves the lungs, lymph nodes and lymphatic ducts. In the lungs, it is characterized by the proliferation of smooth muscle cells around lymphatics in the bronchovascular bundles, lobular septa and pleura The nature of smooth muscle proliferation in PLAM is still unclear. Recently, reactivity of the smooth muscle cells for HMB-45, a melanoma-related antigen has been reported by immunohistochemistry. The purpose of this study was the ultrastructural localization of HMB-45 immunoreactivity in these cells using gold-labeled antibodies.Lung tissue from three cases of PLAM, referred to our Institution for lung transplantation, was embedded in either Poly/Bed 812 post-fixed in 1% osmium tetroxide, or in LR White, without osmication. For the immunogold technique, thin sections were placed on Nickel grids and incubated with affinity purified, monoclonal anti-melanoma antibody HMB-45 (1:1) (Enzo Diag. Co) overnight at 4°C. After extensive washing with PBS, grids were treated with Goat-anti-mouse-IgG-Gold (5nm) (1:10) (Amersham Life Sci) for 1 hour, at room temperature.


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