Diet alters age-related remodeling of aortic collagen in mice susceptible to atherosclerosis

Watson, Shana R.; Cooper, Kara M; Liu, Piaomu; Gharraee, Nazli; Du, Liya; Han, Savannah M; Peña, Edsel A.; Sutton, Michael A.; Eberth, John F.; Lessner, Susan M.

doi:10.1152/ajpheart.00420.2020

Cited by 6 publications

(3 citation statements)

References 60 publications

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“…Mechanical stimulation, as wall stretching, is a physiological process of functioning vascular walls. Calcium deposits negatively correlate with wall elasticity, also up-regulating ECs' expression of MMP-9, IL-6 and CD62e, a marker of macrophage adhesion [67]. Tissue degradation is also preceded by necroptosis and apoptosis in both TAA and AAA [25].…”

Section: Abdominal Aorta Aneurysm-cellular Physiology and Pathophysio...mentioning

confidence: 99%

Cellular, Molecular and Clinical Aspects of Aortic Aneurysm—Vascular Physiology and Pathophysiology

Domagała,

Data,

Szyller

et al. 2024

Cells

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A disturbance of the structure of the aortic wall results in the formation of aortic aneurysm, which is characterized by a significant bulge on the vessel surface that may have consequences, such as distention and finally rupture. Abdominal aortic aneurysm (AAA) is a major pathological condition because it affects approximately 8% of elderly men and 1.5% of elderly women. The pathogenesis of AAA involves multiple interlocking mechanisms, including inflammation, immune cell activation, protein degradation and cellular malalignments. The expression of inflammatory factors, such as cytokines and chemokines, induce the infiltration of inflammatory cells into the wall of the aorta, including macrophages, natural killer cells (NK cells) and T and B lymphocytes. Protein degradation occurs with a high expression not only of matrix metalloproteinases (MMPs) but also of neutrophil gelatinase-associated lipocalin (NGAL), interferon gamma (IFN-γ) and chymases. The loss of extracellular matrix (ECM) due to cell apoptosis and phenotype switching reduces tissue density and may contribute to AAA. It is important to consider the key mechanisms of initiating and promoting AAA to achieve better preventative and therapeutic outcomes.

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Section: Abdominal Aorta Aneurysm-cellular Physiology and Pathophysio...mentioning

confidence: 99%

Cellular, Molecular and Clinical Aspects of Aortic Aneurysm—Vascular Physiology and Pathophysiology

Domagała,

Data,

Szyller

et al. 2024

Cells

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“…The in vivo experiments revealed several interesting findings. First, the atherosclerotic lesion area was increased by conditional CD4 ＋ T-cell JKAP ablation, and collagen fiber, macrophage infiltration, and endothelial hyperplasia were elevated by CD4 ＋ T-cell conditional JKAP ablation, which are hallmarks of atherosclerosis [42][43][44] . However, the JKAP ＋ area in the aortic root was reduced in the conditional JKAPablated mice.…”

Section: The Effect Of Conditional Jkap Ablation In Cd4 ＋ T Cells On ...mentioning

confidence: 99%

JNK Pathway-Associated Phosphatase Deficiency Facilitates Atherosclerotic Progression by Inducing T-Helper 1 and 17 Polarization and Inflammation in an ERK- and NF-κB Pathway-Dependent Manner

Chen,

Fang,

Hong

et al. 2024

JAT

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Aim: JNK pathway-associated phosphatase (JKAP) regulates T cell-mediated immunity and inflammation, which are involved in atherosclerosis pathogenesis. This study investigated the effects of JKAP on T-helper (Th) cell polarization, inflammation, and atherosclerotic progression. Methods: Serum JKAP levels were measured in 30 patients with coronary heart disease (CHD) and 30 controls. CHD blood naïve CD4 ＋ T cells were acquired, followed by JKAP overexpression and knockdown with or without treatment with PD98059 (ERK inhibitor) or BAY-11-7082 (NF-κB inhibitor) in vitro. CD4 ＋ T-cell conditional JKAP ablation mice were established in vivo, followed by the construction of an atherosclerosis model. Results: JKAP was reduced and negatively correlated with the Gensini score, CRP, Th1 cells, Th17 cells, and proinflammatory cytokines in patients with CHD. In vitro, JKAP overexpression suppressed Th1 and Th17 cell differentiation and proinflammatory cytokines, whereas JKAP knockdown exerted the opposite effect; however, JKAP modification did not affect Th2 cell differentiation. Interestingly, JKAP negatively regulated the ERK and NF-κB pathways; meanwhile, the PD98059 and BAY-11-7082 treatments repressed Th1 and Th17 cell differentiation, and attenuated the effect of JKAP knockdown on these indices. In vivo, conditional CD4 ＋ T-cell JKAP ablation increased Th1 and Th17 cell polarization in the spleen, lymph node, blood, and/or aortic root. Furthermore, CD4 ＋ T-cell conditional JKAP ablation exaggerated atherosclerotic lesions in the aorta, elevated CD4 + cell infiltration and proinflammatory cytokines in the aortic root, and activated the ERK and NF-κB pathways in the aortic root. Conclusion: JKAP ablation facilitates atherosclerosis progression by promoting Th1 and 17 polarization and inflammation through regulation of the ERK and NF-κB pathways.

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“…Significantly, the study also indicates that collagen content alone does not correlate with ultimate tensile stress and strain [ 43 ▪▪ ]. In a murine model ( Apoe −/− ), similar changes in aortic adventitial collagen organization was associated with aging, with a skewing towards longitudinal – as opposed to circumferential – orientation in mice given normal chow, curiously enough with the opposite effect in mice on a high-fat diet [ 44 ▪ ].…”

Section: Collagen Structure and Plaque Integritymentioning

confidence: 99%

Extracellular matrix: paving the way to the newest trends in atherosclerosis

Gialeli

Shami

Gonçalves

2021

Current Opinion in Lipidology

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Purpose of review The extracellular matrix (ECM) is critical for all aspects of vascular pathobiology. In vascular disease the balance of its structural components is shifted. In atherosclerotic plaques there is in fact a dynamic battle between stabilizing and proinflammatory responses. This review explores the most recent strides that have been made to detail the active role of the ECM – and its main binding partners – in driving atherosclerotic plaque development and destabilization. Recent findings Proteoglycans-glycosaminoglycans (PGs-GAGs) synthesis and remodelling, as well as elastin synthesis, cross-linking, degradation and its elastokines potentially affect disease progression, providing multiple steps for potential therapeutic intervention and diagnostic targeted imaging. Of note, GAGs biosynthetic enzymes modulate the phenotype of vascular resident and infiltrating cells. In addition, while plaque collagen structure exerts very palpable effects on its immediate surroundings, a new role for collagen is also emerging on a more systemic level as a biomarker for cardiovascular disease as well as a target for selective drug-delivery. Summary The importance of studying the ECM in atherosclerosis is more and more acknowledged and various systems are being developed to visualize, target and mimic it.

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Diet alters age-related remodeling of aortic collagen in mice susceptible to atherosclerosis

Cited by 6 publications

References 60 publications

Cellular, Molecular and Clinical Aspects of Aortic Aneurysm—Vascular Physiology and Pathophysiology

Cellular, Molecular and Clinical Aspects of Aortic Aneurysm—Vascular Physiology and Pathophysiology

JNK Pathway-Associated Phosphatase Deficiency Facilitates Atherosclerotic Progression by Inducing T-Helper 1 and 17 Polarization and Inflammation in an ERK- and NF-κB Pathway-Dependent Manner

Extracellular matrix: paving the way to the newest trends in atherosclerosis

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