[Atherogenesis as an immunoinflammatory process].

V A Nagornev; A N Voskan'iants

Home/Archive/PubMed

PubMed · 15293791

[Atherogenesis as an immunoinflammatory process].

V A Nagornev·A N Voskan'iants

View original source ↗Export metadata ↓

Abstract

The paper contains findings, obtained at the laboratory of atherosclerosis of Anichkov's Research Institute of Experimental Medicine, Russia's Academy of Medical Sciences, during the last decade with the above research results being compared with published data. Atherogenesis is discussed from the standpoint of the development of immune inflammation in the arterial wall. The mechanisms and factors triggering the chain of immunoinflammatory reactions, which provoke and keep up the inflammatory process, are also under discussion. The results are indicative of that the atherosclerosis pathogenesis is equally related both with mLDL and with the reaction developing in the vascular wall.

Explore related subjects

Aorta Apolipoproteins B Autoantibodies Carotid Arteries Coronary Artery Disease Humans Lipid Peroxidation Lipoproteins, HDL English Abstract Journal Article Research Support, Non-U.S. Gov't Review

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

V A Nagornev, A N Voskan'iants. 2004. [Atherogenesis as an immunoinflammatory process].. https://pubmed.ncbi.nlm.nih.gov/15293791/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Surgical management of lung cancer invading the aorta or the superior vena cava.

OBJECTIVE: Invasion of mediastinal structures (T4) is considered as an absolute contraindication to surgical management of non-small cell lung cancer (NSCLC). The authors studied the role of surgical treatment in case of direct aortic and superior venous caval involvement. PATIENTS: From 1995 to 2000, 13 patients with left lung NSCLC invading descending aorta and 9 patients with right upper lobe NSCLC and superior vena cava (SVC) invasion were subjected to thoracotomy for lung resection. Surgery was indicated in case of absence of intraluminal extension. All patients were cN2 negative. The pathology results and 5-year survival were recorded and analyzed. RESULTS: In three cases (23%) the tumor was adhered to the parietal pleura overlying descending aorta, which was resected en block with tumor-associated lung parenchyma. Aortic adventitia invasion by tumor led to local resection of adventitia (<1cm(2)) in nine patients (69%). Invasion deeper than adventitia was encountered in one case (8%), which was managed with aortic partial occlusion, resection of aortic wall and repair of the defect with Gore graft patch. In three patients (33%) the SVC wall was involved by the tumor 1-3cm in length and 2-4mm of the circumference. The defect was repaired with direct suturing. In five patients (56%) the area of SVC wall that was invaded was 3cmx2cm. The defect was repaired with Dacron patch. In 1 patient (11%) an arterial 14 graft was end-to-end interposed. All resections were radical (R0). Neither associated postoperative complications nor operative mortality was recorded. Five-year survival was 30.7% for the cases with aortic invasion and 11% for the ones with SVC involvement. CONCLUSIONS: Radical surgical resection of lung tumors with localized aortic invasion can be considered after exclusion of N2 involvement.

Aorta↗

PubMed2007

Pathogen recognition by Toll-like receptor 2 activates Weibel-Palade body exocytosis in human aortic endothelial cells.

The endothelial cell-specific granule Weibel-Palade body releases vasoactive substances capable of modulating vascular inflammation. Although innate recognition of pathogens by Toll-like receptors (TLRs) is thought to play a crucial role in promotion of inflammatory responses, the molecular basis for early-phase responses of endothelial cells to bacterial pathogens has not fully been understood. We here report that human aortic endothelial cells respond to bacterial lipoteichoic acid (LTA) and synthetic bacterial lipopeptides, but not lipopolysaccharide or peptidoglycan, to induce Weibel-Palade body exocytosis, accompanied by release or externalization of the storage components von Willebrand factor and P-selectin. LTA could activate rapid Weibel-Palade body exocytosis through a TLR2- and MyD88-dependent mechanism without de novo protein synthesis. This process was at least mediated through MyD88-dependent phosphorylation and activation of phospholipase Cgamma. Moreover, LTA activated interleukin-1 receptor-associated kinase-1-dependent delayed exocytosis with de novo protein synthesis and phospholipase Cgamma-dependent activation of the NF-kappaB pathway. Increased TLR2 expression by transfection or interferon-gamma treatment increased TLR2-mediated Weibel-Palade body exocytosis, whereas reduced TLR2 expression under laminar flow decreased the response. Thus, we propose a novel role for TLR2 in induction of a primary proinflammatory event in aortic endothelial cells through Weibel-Palade body exocytosis, which may be an important step for linking innate recognition of bacterial pathogens to vascular inflammation.

Aorta↗

PubMed2007

Mechanical strain induces a persistent upregulation of syndecan-1 expression in smooth muscle cells.

Syndecan-1 belongs to a family of transmembrane proteoglycans, acts as a coreceptor for growth factor binding, as well as cell-matrix and cell-cell interactions, and is induced in smooth muscle cells (SMCs) following balloon catheter injury. In this report, we investigated syndecan-1 expression in SMCs in response to several distinct biomechanical force profiles and the related syndecan shedding response. Syndecan-1 mRNA expression increased in response to 5% and 10% cyclic strain (24 h: 206 +/- 40% and 278 +/- 33%, respectively, P < 0.05) when compared to unstrained controls. When subjected to 10% cyclic strain for periods of up to 48 h, syndecan-1 mRNA levels remained elevated at 294 +/- 31%. Notably, the SMC mechanosensor mechanism remained responsive after an initial 24 h "preconditioning" period, as evident by a fivefold increase in syndecan-1 gene expression following a change in cyclic stress from 10% to 20% (48 h: 516 +/- 55%, P < 0.05). Of note, similar behavior was not observed in an analysis of syndecan-2 mRNA levels. Commensurate with mRNA responses, mechanical stress induced an increase in cell-associated syndecan-1 protein levels with an associated increase in protein shedding. Given the varied functions of syndecan-1, stress-induced effects on SMC syndecan-1 expression and shedding may represent an additional component of the pro-inflammatory, growth-stimulating pathways that are activated in response to changes in the mechanical microenvironment of the vascular wall. Syndecan-1 expression is uniquely influenced by changes in the phase and magnitude of the local stress field.

Aorta↗