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Endothelial Cells and Hemodynamics
Published in Wilmer W Nichols, Michael F O'Rourke, Elazer R Edelman, Charalambos Vlachopoulos, McDonald's Blood Flow in Arteries, 2022
Elazer Edelman, Farhad Rikhtegar Nezami
In a fascinating manner though, despite the fact that the risk factors and pressure and blood exposure resonate throughout the vascular system, atherosclerotic plaques appear in specific locations, and particular plaques seem to destabilize more than others. Atherosclerotic plaque preferentially forms in specific locations—bifurcations, branching points and sharp curves (Ku et al., 1985; Li et al., 2005). Blood flow patterns unify the systemic risk and local emergence of lesions. While the progressive steps in atherosclerosis pathogenesis are complex and still emerging, what is clear is that the interaction of flow and endothelial cell injury are the likely initial factors, followed by lipoprotein deposition, inflammatory reactions and ultimately smooth muscle cell migration for cap formation (Libby et al., 2011). Blood flow is the essential driving force in lesion formation and the response to intervention, and it is these issues we present here.
Radiation Immunology
Published in Kedar N. Prasad, Handbook of RADIOBIOLOGY, 2020
B lymphocytes in mice are relatively more radiosensitive than T lymphocytes after acute or chronic exposure.9 The rate of recovery was similar after chronic exposure.9 It has been reported9 that chronic irradiation caused an immunosuppression that persisted throughout the adult life of the animals. The number of spleenic T and B cells in these mice returned to normal. The phenomenon of cap formation, a process involving surface membrane components, was adversely affected in the surviving B cell population, but not in the surviving T cell population.9 This defect also recovered. Thus, the persistent immunodeficiency in chronically irradiated mice may be due to the fact that the microenvironment of the irradiated spleen alters factors regulating T and B cell interaction in response to a T-dependent antigen.
The Structure of Transcriptons and The Regulation of Transcription
Published in M. Gerald, M.D. Kolodny, Eukaryotic Gene Regulation, 2018
Some contradictory results were obtained in the course of 5′ end studies. Two types of 5′ ends were detected in nuclear RNA. These were triphosphorylated 5′ ends which were formed as a result of conserving α-, β-, and γ-phosphates at the first nucleotide of RNA and capped 5′-ends whose general structure is m7G(5′)ppp(5′)N′mpN″mp. This cap formation is a posttranscriptional process which takes place in the course of processing and involves condensation of the guanylate residue in a 5′-5′ triphosphate linkage followed by methylation of two or three 5′ terminal nucleotides (for references see Perry40).
Role and implications of the CXCL12/CXCR4/CXCR7 axis in atherosclerosis: still a debate
Published in Annals of Medicine, 2021
Hussam A. S. Murad, Misbahuddin M. Rafeeq, Thamer M. A. Alqurashi
Chemokines and their receptors play a key role in the initiation, development, and progression of atherosclerosis. Various cells implicated in atherosclerosis pathogenesis, such as ECs, vascular smooth muscle cells (VSMCs), platelets, macrophages, monocytes and leukocytes, widely express various chemokines and their receptors [11]. Leukocyte movement through the endothelium involves several steps that are regulated by different chemokines and their receptors. Several studies have emphasized the role of different chemokines and their receptors on different stages of atherosclerosis initiation, development and progression [12]. In addition to their modulatory and regulatory functions, some chemokines directly act as adhesion molecules and some influence the phenotype of inflammatory cells. Furthermore, chemokines play a prudent role in the stability of atherosclerotic lesions, through “fibrous cap” formation. Various methodologies are being used to explore the possible roles of chemokines and their receptors in atherosclerosis, including genetic and pharmacological experiments. For example, atherosclerosis was induced in ApoE−/− or Ldlr−/− knockout murine models through vascular injury or a high-fat diet; furthermore, a specific chemokine or receptor was knocked out to ascertain its role in atherosclerosis [13].
Aggravation of atherosclerosis by pulmonary exposure to indium oxide nanoparticles
Published in Nanotoxicology, 2020
Dong-Keun Lee, Hyung Seok Jang, Hyunji Chung, Soyeon Jeon, Jiyoung Jeong, Jae-Hoon Choi, Wan-Seob Cho
The measurement of atherosclerotic lesion size showed that In2O3 NPs treatment significantly increased atherosclerotic lesion formation (Figure 6(A–D)). Moreover, the accumulation of macrophages in the lesion was increased by In2O3 NP treatment (Figure 7). However, Masson’s trichrome staining and immunofluorescence staining of smooth muscle actin showed that fibrous cap formation was not significantly affected by In2O3 NPs (Figure 6(E–H), Supplementary Figure S5). The mRNA expression of cytokines in the aortic tissue was evaluated. The levels of IL-6 and MCP-1 were significantly increased in the In2O3 NP-treated groups, without any dose-dependency, whereas the levels of no other cytokines were significantly different compared to those in the vehicle control (Figure 8).
Pro-resolving lipid mediators in the resolution of neointimal hyperplasia pathogenesis in atherosclerotic diseases
Published in Expert Review of Cardiovascular Therapy, 2019
Mohan Satish, Devendra K Agrawal
Atherosclerosis is a chronic inflammatory process that is most susceptible to occurrence in the intimal layer of arteries, particularly at bifurcation points of the blood vessel. The earliest events of atherosclerosis include activation of the endothelium by certain risk factors such as hypercholesterolemia [1]. In general, in atherosclerotic arteries, the clinical symptoms develop primarily due to two events: (a) The prototypical plaque formation that ensues within the inflammatory milieu results from oxidized lipids creating foam cells, a macrophage derivative [2]. Plaque instability and rupture are attributed to a weakening of its fibrous cap due to matrix degradation by further macrophage secretions (cytokines, chemokines, growth-factors, and disintegrins) [2,3]. Subsequent vessel thrombosis can promote symptomatic stenosis or occlusion underlying the ischemic events seen in stroke of the brain, reduced coronary perfusion of the heart in patients with coronary artery disease (CAD), and limb claudication seen in peripheral arterial disease (PAD) [1], and (b) Following mechanical injury to the endothelium that commonly occur during interventional procedures, including balloon angioplasty and intravascular stenting, circulating leukocytes, monocytes, and T-lymphocytes attach and infiltrate the intima and release mediators to promote smooth muscle cell (SMC) migration towards lumen with fibrous cap formation, resulting in the development of neointimal hyperplasia and restenosis [1,4].