Atherosclerosis non transgenic mice high fat diet

For example, the administration of RvD2 and MaR1 to atheroprone mice promotes polarization of macrophages toward a pro-resolving phenotype Amanda C. Activation of these receptors leads to increased expression of inflammatory pathway enzymes, e. Reference information: Although the these pro-resolving mediators act on distinct receptors, they appear to induce similar atheroprotective mechanisms, including enhanced efferocytosis, pro-resolving macrophage polarization, decreased necrotic core formation, and increased collagen synthesis with thickened fibrous cap development.

Although both groups consumed an equal amount of calorie of each diet, HFFD feeding led to prominent IR accompanied by elevated plasma lipids, hepatic steatosis and adipose accumulation, even though the body weight was unchanged.

The role of non-resolving inflammation in atherosclerosis

SPMs themselves are able to augment and therefore amplify this pathway. Figure S5. In a case-control study, a polymorphism in ALOX15 that was associated with higher enzyme activity was enriched in a population of control subjects without coronary artery disease CAD versus patients with CAD Use of bacterial expression cloning to localize the epitopes for a series of monoclonal antibodies against apolipoprotein B Increased plasma levels of lipids are basically caused by high uptake of free fatty acids into the liver where they can be synthesized into VLDLs, which are accumulated in the plasma.

In further support of this idea, analysis of human carotid plaques revealed that expression of ADAM17 is increased while that of MerTK is decreased in macrophages surrounding the necrotic cores as compared with macrophages in peripheral regions of the plaques Transgenic mice expressing human apoB and apoB Editing of human apolipoprotein B mRNA.

The ADAM17 effect is particularly interesting given that Mer proto-oncogene tyrosine kinase MerTKa key macrophage efferocytosis receptor in atherosclerotic lesions, is cleaved by this protease, resulting in defective lesional efferocytosis As shown in Fig.

However, this enzyme is also involved in the synthesis of lipoxins and resolvins above. Evaluation of lesional development and progression. Curr Opin Lipidol.

Plasma was collected from fasted animals and measured as described in the Methods. It has been shown that small LDLs are more atherogenic than large ones because they are trapped in the arterial intima more easily and become oxidized [ 2526 ].

The changes in plasma glucose levels top left and right and insulin levels bottom left were determined. The concept that 5-LOX is involved in atherosclerosis is also supported by human genetic findings.

First, it lowers MK2 activity, which increases nonphosphorylated 5-LOX and promotes its nuclear-to-cytoplasmic translocation. Blood was drawn at 0 minutes before administration of Triton WR and 2, 4 and 6 hours after Triton WR injection.

We next examined adipose tissue and found that the amount of adipose accumulation of the HFFD group was significantly increased in both subcutaneous 1. Find articles by Cai, B. Expression of human apolipoprotein B in transgenic mice. These combined data suggest that BLT1 signaling is important in early atherogenesis but that other proatherogenic processes become dominant in more advanced atherosclerosis.

Apolipoprotein E: Specific phagocytic receptors binding to phosphatidylserine on apoptotic cells have been implicated in the regulation of efferocytosis in atherosclerotic lesions.Zinc finger nucleases are the most mature and characterized of these tools, and can Sage Labs · Design A Custom Model · Chat Support Available · First for Knockout RatsTransgenic animals (commonly mice or rats) are those that have.

Transgenic mice in which AIF-1 expression is driven by the G/C modified SM22 alpha promoter to restrict AIF-1 expression to VSMC develop significantly increased atherosclerosis compared with wild-type control mice when fed a high-fat diet (P = ).Cited by: A mouse model of human familial hypercholesterolemia: markedly elevated low density lipoprotein cholesterol levels and severe atherosclerosis on a low-fat chow diet.

Nat Med. ; 4: – Crossref Medline Google Scholar; 7 Veniant MM, Pierotti V, Newland D, Cham CM, Sanan DA, Walzem RL, Young SG. Susceptibility to atherosclerosis in mice expressing exclusively apolipoprotein B48 or Cited by: In contrast, transgenic animals on the high-fat diet had extensive atherosclerotic lesions (>microns 2/section) that were widely distributed throughout the proximal 1, microns of the aorta.

Thus, human apo-B expression, in the setting of a diet rich in fats, causes severe atherosclerosis in by: Mice fed high-fat, high-cholesterol diets had a significantly higher incidence of gastritis than mice fed normal chow, 62% versus 5%, respectively (P,).

This effect was specific for LDLR 2/2 mice, because no.

Probing the Genetics of Atherosclerosis in Transgenic Mice

Similarly, transgenic mice overexpressing 12/LOX on the Apoe –/– background and fed a chow diet showed attenuated atherosclerosis progression, which was thought to be due to increased 12/LOX–mediated synthesis of LXA 4.

However, Merched and colleagues demonstrated that the role of 12/LOX in atherosclerosis is not by:

Atherosclerosis non transgenic mice high fat diet
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