scholarly journals Properties of Lysosomes in Atherosclerotic Lesions of Human Aorta

1980 ◽  
Vol 8 (2) ◽  
pp. 321-327
Author(s):  
Masahiro KUROSAKA ◽  
Kazushi HIROHATA ◽  
Masumi USUI ◽  
Kimiko MUTO ◽  
Tsuneo IMANAKA ◽  
...  
Keyword(s):  
Human Aorta ◽  
Atherosclerotic Lesions

Eva1a ameliorates atherosclerosis by promoting re-endothelialization of injured arteries via Rac1/Cdc42/Arpc1b

2020 ◽  
Author(s):  
Jingxuan Li ◽  
Yingyu Chen ◽  
Jianing Gao ◽  
Yue Chen ◽  
Changping Zhou ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Cell Counting ◽  
Human Aorta ◽  
Atherosclerotic Lesions ◽  
Rna Transfection ◽  
Promising Therapeutic Target ◽  
Carotid Artery Injuries ◽  
Underlying Mechanisms ◽  
Interfering Rna ◽  
Novel Protein

Abstract Aims Eva-1 homologue 1 (Eva1a) is a novel protein involved in the regulation of cardiac remodelling and plaque stability, but little is known about its role in re-endothelialization and the development of atherosclerosis (AS). Thus, in the present study, we aimed to elucidate the function of Eva1a in re-endothelialization and AS. Methods and results Wire injuries of carotid and femoral arteries were established in Eva1a−/− mice. Eva1a-deficient mice were crossed with apolipoprotein E−/− (ApoE−/−) mice to evaluate AS development and re-endothelialization of carotid artery injuries. Denudation of the carotid artery at 3, 5, and 7 days was significantly aggravated in Eva1a−/− mice. The neointima of the femoral artery at 14 and 28 days was consequently exacerbated in Eva1a−/− mice. The area of atherosclerotic lesions was increased in Eva1a−/−ApoE−/− mice. To explore the underlying mechanisms, we performed transwell, scratch migration, cell counting kit-8, and bromodeoxyuridine assays using cultured human aorta endothelial cells (HAECs), which demonstrated that EVA1A promoted HAEC migration and proliferation. Proteomics revealed that the level of actin-related protein 2/3 complex subunit 1B (Arpc1b) was decreased, while Eva1a expression was absent. Arpc1b was found to be a downstream molecule of EVA1A by small interfering RNA transfection assay. Activation of Rac1 and Cdc42 GTPases was also regulated by EVA1A. Conclusion This study provides insights into anti-atherogenesis effects of Eva1a by promoting endothelium repair. Thus, Eva1a is a promising therapeutic target for AS.

Quantitative analysis of the expression of caspase 3 and caspase 9 in different types of atherosclerotic lesions in the human aorta

2015 ◽  
Vol 99 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Igor A. Sobenin ◽  
Yuri V. Bobryshev ◽  
Gleb A. Korobov ◽  
Evgeny N. Borodachev ◽  
Anton Y. Postnov ◽  
...  
Keyword(s):  
Quantitative Analysis ◽  
Caspase 3 ◽  
Human Aorta ◽  
Caspase 9 ◽  
Atherosclerotic Lesions ◽  
Different Types

scholarly journals Flow patterns and preferred sites of atherosclerotic lesions in the human aorta – I. Aortic arch

Biorheology ◽  
2014 ◽  
Vol 51 (4-5) ◽  
pp. 239-255 ◽  
Author(s):  
Shunsuke Endo ◽  
Harry L. Goldsmith ◽  
Takeshi Karino
Keyword(s):  
Aortic Arch ◽  
Flow Patterns ◽  
Human Aorta ◽  
Atherosclerotic Lesions

scholarly journals The Interaction of Plasma Sialylated and Desialylated Lipoproteins with Collagen from the Intima and Media of Uninvolved and Atherosclerotic Human Aorta

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Igor A. Sobenin ◽  
Igor V. Suprun ◽  
Vasiliy P. Karagodin ◽  
Alexander S. Feoktistov ◽  
Alexandra A. Melnichenko ◽  
...  
Keyword(s):  
Normal Tissue ◽  
Human Aorta ◽  
Fatty Streak ◽  
Atherosclerotic Lesions

We have evaluated the binding of sialylated and desialylated lipoproteins to collagen isolated from the proteoglycan and musculoelastic layers of intima and media of uninvolved human aorta and atherosclerotic lesions. Comparing various collagen preparations from the uninvolved intima-media, the binding of sialylated apoB-containing lipoproteins was best to collagen from the intimal PG-rich layer. Binding of sialylated apoB-containing lipoproteins to collagen from this layer of fatty streak and fibroatheroma was 1.4- and 3.1-fold lower, respectively, in comparison with normal intima. Desialylated VLDL versus sialylated one exhibited a greater binding (1.4- to 3.0-fold) to all the collagen preparations examined. Desialylated IDL and LDL showed a higher binding than sialylated ones when collagen from the intimal layers of fibroatheroma was used. Binding of desialylated HDL to collagen from the intimal PG-rich layer of normal tissue, initial lesion, and fatty streak was 1.2- to 2.0-fold higher compared with sialylated HDL.

Adrenomedullin in monocytes and macrophages: possible involvement of macrophage-derived adrenomedullin in atherogenesis

1999 ◽  
Vol 97 (2) ◽  
pp. 247-251 ◽  
Author(s):  
Masaharu NAKAYAMA ◽  
Kazuhiro TAKAHASHI ◽  
Osamu MURAKAMI ◽  
Hiroshi MURAKAMI ◽  
Hironobu SASANO ◽  
...  
Keyword(s):  
Northern Blot ◽  
Blot Analysis ◽  
Northern Blot Analysis ◽  
Human Aorta ◽  
Atherosclerotic Lesions ◽  
Potent Vasodilator ◽  
Monocytes And Macrophages ◽  
The Media ◽  
And Migration ◽  
Progression Of Atherosclerosis

Macrophages secrete a variety of growth factors, cytokines and vasoactive peptides, which are related to the progression of atherosclerosis. Adrenomedullin (ADM) is a potent vasodilator peptide and inhibits proliferation and migration of vascular smooth muscle cells. In this study, we investigated the production and secretion of ADM by monocytes and macrophages by Northern blot analysis, RIA and immunocytochemistry. Northern blot analysis showed that ADM mRNA was expressed in human monocytes obtained from peripheral blood and monocyte-derived macrophages. The expression level of ADM mRNA in monocyte-derived macrophages was about five times higher than that in monocytes. Treatment with lipopolysaccharide (100 ng/ml) for 24 h increased ADM mRNA expression levels in both monocytes and monocyte-derived macrophages. The levels of immunoreactive ADM in the media of monocyte-derived macrophages were about three times higher than that of monocytes (0.718±0.046 fmol/24 h/105 cells, n = 8 compared with 0.259±0.018 fmol/24 h/105 cells, n = 8; mean±S.E.M., P < 0.01). The secretion was also increased by treatment with lipopolysaccharide. Immunocytochemistry showed positive ADM immunostaining in macrophages in atherosclerotic lesions of human aorta obtained at autopsy. ADM secreted from activated macrophages may play an inhibitory role in atherogenesis.

Morphological and Crystal-Chemical Features of Macro- and Microcalcifications of Human Aorta

2021 ◽  
pp. 1-8
Author(s):  
Inna-Margaryta Radomychelski ◽  
Artem Piddubnyi ◽  
Sergey Danilchenko ◽  
Olena Maksymova ◽  
Yuliia Moskalenko ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Human Aorta ◽  
Control Group ◽  
Ectopic Calcification ◽  
Aortic Tissue ◽  
Macroscopic Description ◽  
X Ray ◽  
Atherosclerotic Lesions ◽  
Transmission Electron

Ectopic calcification or pathological biomineralization correlates with morbidity and mortality from cardiovascular diseases. Aortas with atherosclerotic lesions and biomineralization were selected for the study. Thirty samples of mineralized abdominal aortas (group M) were examined by histology. Depending on the calcifications size, samples were separated into group M1 (macroscopic calcifications) and M2 (microscopic calcifications). Each group consists of 15 samples. Calcification 2 mm or less were considered as microscopic, >2 mm—macroscopic. Thirty samples of aortic tissue without biomineralization (group C) were used as a control group. Aortic tissue was examined by macroscopic description, histology, histochemistry, immunohistochemistry (IHC), scanning electron microscopy (SEM) with microanalysis, and transmission electron microscopy (TEM). The results of IHC showed the involvement of OPN in the formation and development of pathological biomineralization, but the obvious role of OPN in the differentiation of macro- and microcalcifications of atherosclerotic aorta was not revealed. SEM with X-ray microanalysis confirmed that the biomineral part of the aortic samples of the M1 group consisted mainly of apatites, which correspond to previous studies. The Ca/P ratio was less in the M2 group than in the M1 group. It means that microcalcifications can be formed by more defective (immature) hydroxyapatite.

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