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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetes mellitus is a major risk factor for atherosclerosis. Since endothelial alteration is probably associated with the development of atherosclerosis, we questioned whether morphological evidence of endothelial injury could be observed during the first 6 months of diabetes induced by a single intravenous injection of alloxan in normally fed rabbits compared with age-matched controls. Diabetes (plasma glucose greater than 16 mM) was established by 5 days after alloxan injection. Endothelial alterations consistent with injury, including adhesion of white blood cells, platelets, and fibrin-like material to the endothelial surface, were seen in diabetic rabbit aortas by 2 weeks. These alterations became more severe during the next 6 months. Increased endothelial replication in diabetic vessels was shown by the uptake of tritium-labeled thymidine at 2 weeks and at 3 and 6 months. Hyperplasia of intimal smooth muscle cells progressed during 3 months after treatment. About one third of the diabetic rabbits also showed an elevated plasma cholesterol level, which correlated with increased intimal proliferation but not with endothelial injury or replication. The onset of alloxan-induced diabetes in rabbits is associated with nondenuding endothelial injury and subsequent intimal hypertrophy, changes that are consistent with atherogenesis.
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PMID:Intimal alterations in rabbit aortas during the first 6 months of alloxan-induced diabetes. 202 93

Arteries predisposed and resistant to atherosclerosis development were studied. Arteries predisposed to atherosclerosis show a high degree of intima hyperplasia and various alterations of elastic structures. Hyperplasia of the vascular intima followed by disturbance of plasma perfusion through the arterial wall and increase of its cellularity (lymphocytes, monocytes/macrophages) determines possibility of atherosclerosis development (crucial factor of atherosclerosis pathogenesis) in man. Accumulation of lipids in the intima occurs not only in pronounced disturbances of lipid metabolism but at its "normal" indices as well this resulting in atherosclerosis development in all members of the population.
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PMID:[The role of hyperplasia of the arterial intima in human atherogenesis]. 994 97

Morphological study of intraoperative biopsies of radial and internal mammary arteries taken from patients with ischemic heart disease during coronary bypass surgery revealed structural alterations of intima and media mostly in radial artery. These alterations depended on severity of arterial hypertension, presence of diabetes and extent of atherosclerosis. Hyperplasia of intima could be a basis for radial artery spasm and cause of graft stenoses and occlusions. Therefore protocols of pre and post operative care should take into consideration individual risk factors and morphological and functional features of an artery used for grafting.
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PMID:[Clinical value of morphological analysis of radial and internal mammary arteries in patients with ischemic heart disease]. 1515 15

Hyperplasia and hypertrophy of fat cells can be found in obesity, and increased adiposity is associated with endothelial dysfunction as an early event of atherosclerosis. However, it is unclear whether human adipocytes directly influence endothelial function. To study the crosstalk between fat and endothelial cells, human umbilical venous endothelial cells (HUVECs), and human coronary artery endothelial cells (HCAECs) were cultured in infranatants (Adipo) of primary differentiated human adipocytes. Interestingly, incubation of HUVECs and HCAECs with Adipo significantly increased monocyte adhesion 7.3 and 2.2-fold, respectively. VCAM-1, ICAM-1, and E-selectin in HUVECs were upregulated 3.9, 3.0, and 9.5-fold, respectively, under these conditions. Furthermore, Adipo significantly stimulated NFkappaB activity 1.9-fold. The NFkappaB inhibitor MG-132 and heat inactivation significantly reversed Adipo-stimulated monocyte adhesion. TNFalpha-neutralizing antibodies partly reversed Adipo-induced monocyte adhesion. In contrast, thiazolidinedione-pretreatment of human adipocytes did not alter the effects of Adipo. Adipo did not show cytotoxic effects. Taken together, we demonstrate that endothelial dysfunction is induced by adipocyte-secreted factors via NFkappaB partly dependent on TNFalpha.
Atherosclerosis 2008 Feb
PMID:Secretory products from human adipocytes impair endothelial function via nuclear factor kappaB. 1760 62

Development of a cultured tissue experimental model of rat aorta was explored in order to study mechanism of vascular smooth muscle (VSMC) proliferation. This particular model has potential with regard to amelioration of atherosclerosis and other vascular diseases in comparison to whole animal and cell culture models. The aorta segments of rats were divided into 4 experimental groups: the injured endothelium, injured endothelium plus BQ123, without injured endothelium and without injured endothelium plus BQ123. Each of group was subdivided into a further 2 subgroups and cultured with 20% serum and with serum-free DMEM. Each group cultured in vitro for 5, 8 and 13 days respectively. The control group was not cultured in vitro. Bromodeoxyuridine (BrDU 8x10(-4) mol/l) was added into the cultured medium of all groups, 24 h prior to harvesting. These segments were fixed in 4% paraformaldehyde for paraffin slice used to HE and immunocytochemical staining and other aorta segments were used to detect the expressions of hypertension-related gene-1 (HRG-1) and smooth muscle 22 alpha (SM22alpha) by RT-PCR. ET-1 content in the supernatant was detected with radioimmunology. Proliferous VSMC can be observed on artery segments cultured in vitro, and conspicuous plaques were developed on model vascular wall cultured for 13 days. Labeled cells increased with an increase in culture time but were not seen in the control group. A greater number of labeled cells were observed in injured endothelium group cultured in 20% serum DMEM. Hyperplasia was inhibited after BQ123 was added into the medium, suggesting that serum and ET-1 are important factors that lead to VSMC proliferation. Expressions of HRG-1 and SM22alpha were decreased while the aorta segments were cultured in vitro, minimum or even absent mRNA expressions of HRG-1 and SM22alpha were detected in injured endothelium cultured in 20% serum DMEM and increased in injured endothelium plus BQ123 group cultured. ET-1 content in the supernatant increased in injured endothelium cultured in 20% serum DMEM. These results show that the phenotypic transform and VSMC proliferation on cultured artery segments were related not only to serum culture, but also to ET-1 secreting. ET-1 and serum may be the main factors of contributing to the proliferation and phenotypic transform. This model provides a favorable experimental platform for research into the mechanism of vascular proliferous diseases as well as its prevention and treatment.
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PMID:A novel cultured tissue model of rat aorta: VSMC proliferation mechanism in relationship to atherosclerosis. 1793 23

Hyperplasia and hypertrophy of fat cells can be found in obesity and increased adiposity is associated with endothelial dysfunction as an early event of atherosclerosis. However, it is unclear whether human adipocytes directly influence endothelial protein secretion. To study the crosstalk between fat and endothelial cells, human umbilical venous endothelial cells (HUVECs) were cultured in infranatants (Adipo) of primary differentiated human adipocytes. Interestingly, significantly increased secretion of 23 cytokines and chemokines from HUVECs was detected in four independent experiments after Adipo stimulation by protein array analysis detecting a total of 174 different proteins. Among those, time-dependent Adipo-induced upregulation of cytokine secretion in HUVECs was confirmed by ELISA for interleukin (IL)-8, monokine induced by gamma interferon, macrophage inflammatory protein (MIP)-1beta, MIP-3alpha, monocyte chemoattractant protein-1, and IL-6. Factors besides adiponectin, leptin, resistin, and tumor necrosis factor alpha appear to mediate these stimulatory effects. Our findings suggest that endothelial cell secretion is significantly influenced towards a proinflammatory pattern by adipocyte-secreted factors.
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PMID:Secretory products from human adipocytes stimulate proinflammatory cytokine secretion from human endothelial cells. 1917 2