Modelos experimentales de aterosclerosis

Santos‐Gallego, Carlos G.; Badimón, Juan J.; Ibáñez, Borja

doi:10.1016/s1131-3587(13)70087-6

Cited by 5 publications

(4 citation statements)

References 59 publications

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“…In addition, while the ApoE −/− model on a high fat diet provides accelerated development of plaques and has been extensively characterized, the cholesterol levels developed in this model are much higher than seen in humans. It may be useful to consider an alternative model such as the LDLR −/− mouse, which develops cholesterol levels closer to those observed in humans [21]. Lowering cholesterol levels and measuring GCX, EC apoptosis, and MMP-9 at several time points may help to further clarify the relative importance of systemic and local factors in atherogenesis.…”

Section: Discussionmentioning

confidence: 99%

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Endothelial glycocalyx, apoptosis and inflammation in an atherosclerotic mouse model

et al. 2016

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Background and aims Previous experiments suggest that both increased endothelial cell apoptosis and endothelial surface glycocalyx shedding could play a role in the endothelial dysfunction and inflammation of athero-prone regions of the vasculature. We sought to elucidate the possibly synergistic mechanisms by which endothelial cell apoptosis and glycocalyx shedding promote atherogenesis. Methods 4- to 6-week old male C57Bl/6 apolipoprotein E knockout (ApoE−/−) mice were fed a Western diet for 10 weeks and developed plaques in their brachiocephalic arteries. Results Glycocalyx coverage and thickness were significantly reduced over the plaque region compared to the non-plaque region (coverage plaque: 71±23%, non-plaque: 97±3%, p= 0.02; thickness plaque: 0.85±0.15 μm, non-plaque: 1.2±0.21 μm, p= 0.006). Values in the non-plaque region were not different from those found in wild type mice fed a normal diet (coverage WT: 92±3%, p= 0.7 vs. non-plaque ApoE−/−, thickness WT: 1.1±0.06 μm, p= 0.2 vs. non-plaque ApoE−/−). Endothelial cell apoptosis was significantly increased in ApoE−/− mice compared to wild type mice (ApoE−/− :64.3±33.0, WT: 1.1±0.5 TUNEL-pos/cm, p= 2×10−7). The number of apoptotic endothelial cells per unit length was 2 times higher in the plaque region than in the non-plaque region of the same vessel (p= 3×10−5). Increased expression of matrix metalloproteinase 9 co-localized with glycocalyx shedding and plaque buildup. Conclusions Our results suggest that, in concert with endothelial apoptosis that increases lipid permeability, glycocalyx shedding initiated by inflammation facilitates monocyte adhesion and macrophage infiltration that promote lipid retention and the development of atherosclerotic plaques.

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Section: Discussionmentioning

confidence: 99%

“…We also excised the brachiocephalic branch where disease commonly localizes and plaque rupture ultimately occurs [21, 22]. Excised vessels were frozen in a block of optimal cutting temperature (OCT) compound, stored at −80°C, and later sectioned (6μm thick sections) to expose the vessel wall cross-section using a cryostat set at −20°C.…”

Section: Methodsmentioning

confidence: 99%

Endothelial glycocalyx, apoptosis and inflammation in an atherosclerotic mouse model

et al. 2016

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“…Rats are classified as an HDL mammal, because, unlike humans, these lipoproteins predominate in its plasma (Chapman, 1986). In addition, the cholesterol ester transfer protein, which plays an important role in human lipoprotein profiles, is absent in the rat (Santos-Gallego et al, 2013). These main differences are the reason why, despite a hyperlipidic and hypercaloric diet were provided, the rats developed only abnormalities of an apparently initial stage or prior to atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

Impact of endodontic and periodontal diseases and treatments on the aorta and liver of obese and non‐obese rats

et al. 2021

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To evaluate the impact of the presence and treatment of periodontal disease (PD) and apical periodontitis (AP) on the aorta and liver of obese and non-obese rats.Methodology: One hundred and forty Wistar rats were divided into two groups, according to the diet administered: normal diet (-n), without obesity; and cafeteria diet (-c), with induced obesity. These groups were divided into seven subgroups according to the specific experimental protocols: naïve control (NC); AP; AP with treatment (APt); PD; PE with treatment (PDt); AP and PD (APPD); and AP and PD with treatment (APPDt). AP and PD lesions were induced for four weeks. Four weeks after treatments, the animals were euthanatized, and the aorta and liver were dissected for histological evaluation. For the comparison of the thickness of the aorta between groups, the Kruskal-Wallis test was used, followed by the Mann-Whitney test. For the analysis of other variables related to the aorta and liver outcomes, logistic regression was carried out.Results: Both PD and AP were associated with the development of histological alterations in the aortic arch, with no significant difference between obese and non-obese animals (p = .17). The aorta thickness was increased significantly (p < .05) with the combination of PD and AP in obese rats (APPDt-c group) compared with the other groups (NC-n, APt-n, APt-c and AP-c). The logistic regression models revealed that the untreated (OR = 7.78; 95%CI = 2.4-25) and treated (OR = 2.9; 95%CI = 1.0-8.4) groups were significantly more likely to have endothelial alterations compared with the control groups (p = .002). Obesity (OR = 16.5; 95%CI = 3.4-81.3) was the only predictor variable of liver steatosis (p < .001). Conclusion:Histological alterations in the aortic arch of obese and non-obese rats were observed in the presence of periodontal disease and apical periodontitis. The combination of PD and AP increased the aorta thickness in obese rats. A reduction of vascular endothelial lesions was observed with the treatments of PD and AP.

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“…Since MafB knockout (KO) mice die in the early postnatal period due to developmental anomalies of neurons in the respiratory center [22], the authors previously generated transgenic mice with macrophage-specific dominant negative MafB by using the macrophage scavenger receptor enhancer promoter [23]. For the present work, the authors specifically crossed these doublenegative MafB mice with apoE-KO mice, a universally accepted animal model of experimental atherosclerosis [24]. There was no significant difference in atherosclerosis extension either using Oil Red O staining of aortic root cross-sections or Sudan-IV staining of the en face aorta.…”

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confidence: 99%

Modelos experimentales de aterosclerosis

Cited by 5 publications

References 59 publications

Endothelial glycocalyx, apoptosis and inflammation in an atherosclerotic mouse model

Endothelial glycocalyx, apoptosis and inflammation in an atherosclerotic mouse model

Impact of endodontic and periodontal diseases and treatments on the aorta and liver of obese and non‐obese rats

MafB and the role of macrophage apoptosis in atherosclerosis: A time to kill, a time to heal

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