High Fat Diet Induces Adhesion of Platelets to Endothelium in Two Models of Dyslipidemia

Abstract

Cardiovascular diseases (CVD) represent about 30% of all global deaths. It is currently accepted that, in the atherogenic process, platelets play an important role, contributing to endothelial activation and modulation of the inflammatory phenomenon, promoting the beginning and formation of lesions and their subsequent thrombotic complications. The objective of the present work was to study using immunohistochemistry, the presence of platelets, monocytes/macrophages, and cell adhesion molecules (CD61, CD163, and CD54), in two stages of the atheromatous process. CF-1 mice fed a fat diet were used to obtain early stages of atheromatous process, denominated early stage of atherosclerosis, and ApoE−/− mice fed a fat diet were used to observe advanced stages of atherosclerosis. The CF-1 mice model presented immunostaining on endothelial surface for all three markers studied; the advanced atherosclerosis model in ApoE−/− mice also presented granular immunostaining on lesion thickness, for the same markers. These results suggest that platelets participate in atheromatous process from early stages to advance d stages. High fat diet induces adhesion of platelets to endothelial cells in vivo. These findings support studying the participation of platelets in the formation of atheromatous plate.

Protective Effect of α-Linolenic Acid on Non-Alcoholic Hepatic Steatosis and Interleukin-6 and -10 in Wistar Rats

“…A diet rich in SFA is related to a chronic pro-inflammatory state that directly or indirectly affects platelet function [13,51]. Therefore, to evaluate the functional characteristics of platelets, we investigated the activity of enzymes of the purinergic system that participate in regulation of the stimulus to platelet aggregability, considering the E-NTPDase and E-5 -nucleotidase enzymes, which are involved in the metabolism of the extracellular ATP and its conversion to ADP, AMP, and adenosine [52].…”

“…The profile of consumed FAs also affects the platelet function and potential stimuli of the formation of thrombi and atheromas. In the formation of atheromatous plaque, the platelets play an essential role, promoting endothelial activation, modulation of the inflammatory phenomenon, and start the formation of lesions and their subsequent thrombotic complications [13].…”

Comparative proteomic analysis of membrane microdomains isolated from two hyperlipidemic animal models

“…The documented depletion of the ApoE gene and the consequently absence of its protein encoding product is enough to lead to the significant increase of circulating lipids and development of atherosclerotic plaques [11][12][13]. Nonetheless, we chose to add a supplementary stress factor, the high fat diet to accelerate the development of atherosclerotic lesions [23,24]. For proteomic comparative study it was selected the hyperlipidemic Golden Syrian hamster, which under a high fat diet was proven to develop atherosclerosis, very similar with the human pathology [3,4,25].…”

Thrombosis, Atherosclerosis and Atherothrombosis - New Insights and Experimental Protocols

“…Furthermore, platelets with their pro-atherogenic potential are regarded as discrete immune cells [7,8]. They can accumulate lipids in the hypercholesterolemic environment and are involved in the early phase of atheromatous formation [9]. Oxidized low-density lipoproteins (ox-LDLs) are suggested to be implicated in the early phase of atherosclerosis by recruiting inflammatory cells in the subendothelium that elucidate the thrombotic process [10].…”