The content of collagen type II in human arteries is correlated with the stage of atherosclerosis and calcification foci

Kuzan, Aleksandra; Chwiłkowska, Agnieszka; Pezowicz, Celina; Witkiewicz, Wojciech; Gamian, Andrzej; Maksymowicz, Krzysztof; Kobielarz, Magdalena

doi:10.1016/j.carpath.2017.02.003

Cited by 27 publications

(13 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Investigations have shown that Rg3 can reverse the M1 polarization to the M2 phenotype in diabetic conditions to repress the occurrence of diabetes-complicated atherosclerosis (Guo et al, 2018), our further experiments confirmed that HFD for 12 weeks lead to plenty of atherosclerotic plaque formation in aorta of ApoE −/− mice, accompanied by abnormal lipoprotein profiles in serum, while Rg3 decreased LDL level and increased HDL level in serum of ApoE −/− mice, inhibited atherosclerotic plaque formation obviously. Furthermore, the arterial wall contains a large amount of collagens, mainly including collagens I, III, V, and XIII (specific existence and endothelial cells) to ensure the elasticity of blood vessels, and maintain the stability of AS plaque, the decrease of collagens can make stable plaque become unstable plaque, then increase the risk of thrombosis (Copes et al, 2019), our results showed aortic collagens contents of AS mice were decreased, while significantly increased in Rg3 treated mice; it is also noted the expression of collagen in atherosclerotic plaques of AS mice increased significantly, study revealed that collagen II contents which mainly exist in cartilage would be increased in atherosclerotic plaques where cholesterol clefts and crystals were present, and relate to lipid core calcification (Kuzan et al, 2017). Meanwhile, Rg3 significantly decreased macrophage aggregation, increased contractile vascular smooth muscle cells (the marker protein is a-SMA) in mice aorta, these results suggest that Rg3 potentially protects against AS caused by abnormal lipid metabolism.…”

Section: Discussionmentioning

confidence: 55%

Ginsenoside Rg3 Alleviates ox-LDL Induced Endothelial Dysfunction and Prevents Atherosclerosis in ApoE−/− Mice by Regulating PPARγ/FAK Signaling Pathway

Geng

et al. 2020

Front. Pharmacol.

View full text Add to dashboard Cite

The initiation of atherosclerosis (AS) induced by dyslipidemia is accompanied by endothelial dysfunction, including decreased healing ability and increased recruitment of monocytes. Studies showed ginsenoside Rg3 has potential to treat diseases associated with endothelial dysfunction which can protects against antineoplastic drugs induced cardiotoxicity by repairing endothelial function, while the effect and mechanism of Rg3 on dyslipidemia induced endothelial dysfunction and AS are not clear. Therefore, we investigated the effects of Rg3 on oxidized low-density lipoprotein (ox-LDL) induced human umbilical vein endothelial cells (HUVECs) dysfunction and high-fat diets (HFD) induced atherosclerosis in ApoE −/− mice, as well as the mechanism. For in vitro assay, Rg3 enhanced healing of HUVECs and inhibited human monocytes (THP-1) adhesion to HUVECs disturbed by ox-LDL, down-regulated focal adhesion kinase (FAK)-mediated expression of vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1); restrained the FAK-mediated non-adherent dependent pathway containing matrix metalloproteinase (MMP)-2/9 expression, activation of nuclear factorkappa B (NF-kB), high mRNA levels of monocyte chemotactic protein 1 (MCP-1) and interleukin 6 (IL-6), besides Rg3 up-regulated peroxisome proliferators-activated receptor g (PPARg) in ox-LDL-stimulated HUVECs. GW9662, the PPARg-specific inhibitor, can repressed the effects of Rg3 on ox-LDL-stimulated HUVECs. For in vivo assay, Rg3 significantly reduced atherosclerotic pathological changes in ApoE −/− mice fed with HFD, up-regulated PPARg, and inhibited activation FAK in aorta, thus inhibited expression of VCAM-1, ICAM-1 in intima. We conclude that Rg3 may protect endothelial cells and inhibit atherosclerosis by up-regulating PPARg via repressing FAK-mediated pathways, indicating that Rg3 have good potential in preventing dyslipidemia induced atherosclerosis.

show abstract

Section: Discussionmentioning

confidence: 55%

Ginsenoside Rg3 Alleviates ox-LDL Induced Endothelial Dysfunction and Prevents Atherosclerosis in ApoE−/− Mice by Regulating PPARγ/FAK Signaling Pathway

Geng

et al. 2020

Front. Pharmacol.

View full text Add to dashboard Cite

show abstract

“…Hardening of the arteries in elderly suggests that the amount of collagen increases and the amount of elastin decreases with age and progression of the atherosclerosis, but experimental data do not allow for unambiguous confirmation of such hypothesis [ 6 – 10 ]. We have previously described the relationship between collagen type II and the degree of atherosclerosis [ 11 ] and among other types of collagen and degree of disease (unpublished data). This is work where our focus is on the products of advanced glycation associated with extracellular matrix proteins.…”

Section: Introductionmentioning

confidence: 99%

Advanced glycation end products as a source of artifacts in immunoenzymatic methods

et al. 2018

Self Cite

View full text Add to dashboard Cite

The most abundant proteins in the arteries are those of extracellular matrix, ie. collagen and elastin. Due to their long half-lifes these proteins have an increased chance to undergo glycation. The aim of this study was to determine relationship between the content of the main extracellular matrix proteins and the advanced glycation end products (AGEs) in arteries. In this study 103 fragments of aorta were analyzed by ELISA and immunobloting for the content of collagens type I, III and IV and elastin and the content of advanced glycation end-products (AGE). A negative correlation between the content of collagens type III and IV and AGE (r = −0,258, p = 0,0122, and a weak negative correlation between collagen type III and age of the sample donor (r = 0,218, p = 0,0262) were demonstrated. This result comes as a surprise and it contradicts an intuitive assumption that with more glycation substrate, i.e. matrix proteins, more AGE products are expected. We have concluded that the results of the ELISA tests must have been influenced by the glycation. As a consequence, either modified protein molecules were not being recognized by the antibodies, or the glycation, and formation of crosslinks have blocked access of the antibodies to the antigen. It will conceal the effect of the linear dependence between the result (absorbance/densitometry) from the quantity of protein to which the antibody is directed.

show abstract

“…Despite the fact that the performed correlation analyses accurately reflect the dependence of individual mechanical parameters on the contents of load-bearing structural components, this dependence is not exhaustive. Assuming that, unlike in the remodelling of arterial walls during the development of atherosclerosis [14], [17], no atypical formations appear in the structure of AAAs as a result of remodelling, there are at least several properties of the fibrotic extracellular matrix that can significantly affect the mechanical properties and parameters of material models. These include, among others, the degree of collagen crosslinking, collagen turn-over, degree of collagen packing, fragmentation of elastic lamellae, degree of hydration (proteoglycan content), and spatial fibre arrangement, described here by the angle between the circumferential direction and the main directions of the fibres ().…”

Section: Discussionmentioning

confidence: 99%

“…Both normal and aneurysmal arterial tissues subjected to uniaxial loading exhibit strong nonlinear behaviour with an exponential stiffening effect at high-strain domains that is typical of soft tissues [12], [14]- [17]. Arterial walls are considered anisotropic, incompressible [2], and subjected to finite strains with negligible shear deformation [13], [21].…”

Section: Introductionmentioning

confidence: 99%

Effect of collagen fibres and elastic lamellae content on the mechanical behaviour of abdominal aortic aneurysms

Kobielarz

2020

Acta Bioeng Biomech

Self Cite

View full text Add to dashboard Cite

Purpose: The main purpose of this study was a detailed analysis of the mechanical and structural characteristics of human abdominal aneurysms in comparison with normal abdominal aortae and determination of the correlations between their mechanical behaviour and the microstructural content. Methods: Various mechanical properties, i.e., mechanical failure properties, elastic moduli, inflection point coordinates, index of anisotropy and incompressibility were determined under uniaxial loading conditions in the circumferential and axial directions. Constitutive parameters were derived from the commonly used constitutive model proposed by Holzapfel et al. [9]. The microstructural arrangement was examined by histological staining supported by scanning electron microscopy analysis. The content of collagen fibres and elastic lamellae was tested in relation to mechanical properties and constitutive parameters. Results: Significant differences were found in the microstructural arrangement and layer composition of the aneurysmal specimens, compared to the normal aorta group. The mechanical properties and constitutive parameters of the aneurysmal specimens were significantly altered, indicating a weakening of the load-bearing properties of the walls of the aneurysms. A comparative analysis discovered significant correlations between structural composition and mechanical parameters, in particular with respect to the number of collagen fibres and failure stress, which can be important for clinical evaluation of abdominal aortic aneurysm (AAA) rupture. Conclusions: Changes in the content of collagen fibres and elastic lamellae correlate with mechanical and constitutive parameters, indicating AAA severity.

show abstract

The content of collagen type II in human arteries is correlated with the stage of atherosclerosis and calcification foci

Cited by 27 publications

References 30 publications

Ginsenoside Rg3 Alleviates ox-LDL Induced Endothelial Dysfunction and Prevents Atherosclerosis in ApoE−/− Mice by Regulating PPARγ/FAK Signaling Pathway

Ginsenoside Rg3 Alleviates ox-LDL Induced Endothelial Dysfunction and Prevents Atherosclerosis in ApoE−/− Mice by Regulating PPARγ/FAK Signaling Pathway

Advanced glycation end products as a source of artifacts in immunoenzymatic methods

Effect of collagen fibres and elastic lamellae content on the mechanical behaviour of abdominal aortic aneurysms

Contact Info

Product

Resources

About