[HTML][HTML] Increased inflammation, endoplasmic reticulum stress and oxidative stress in endothelial and macrophage cells exacerbate atherosclerosis in ApoCIII …
H Yingchun, M Yahong, W Jiangping, H Xiaokui… - Lipids in Health and …, 2018 - Springer
H Yingchun, M Yahong, W Jiangping, H Xiaokui, Z Xiaohong
Lipids in Health and Disease, 2018•SpringerBackground Overexpression of apolipoprotein CIII (ApoCIII) leads to hypertriglyceridemia
(HTG) which promotes atherosclerosis development. However, it remains unclear whether
ApoCIII affects the atherosclerosis alone by promoting the inflammation and endoplasmic
reticulum (ER) stress, or in combination with HTG. Methods Transgenic (ApoCIIItg) mouse
models were used to investigate the atherogenic role of ApoCIII. Since endothelial cells and
macrophages play crucial roles in atherosclerosis, we examined whether triglyceride-rich …
(HTG) which promotes atherosclerosis development. However, it remains unclear whether
ApoCIII affects the atherosclerosis alone by promoting the inflammation and endoplasmic
reticulum (ER) stress, or in combination with HTG. Methods Transgenic (ApoCIIItg) mouse
models were used to investigate the atherogenic role of ApoCIII. Since endothelial cells and
macrophages play crucial roles in atherosclerosis, we examined whether triglyceride-rich …
Background
Overexpression of apolipoprotein CIII (ApoCIII) leads to hypertriglyceridemia (HTG) which promotes atherosclerosis development. However, it remains unclear whether ApoCIII affects the atherosclerosis alone by promoting the inflammation and endoplasmic reticulum (ER) stress, or in combination with HTG.
Methods
Transgenic (ApoCIIItg) mouse models were used to investigate the atherogenic role of ApoCIII. Since endothelial cells and macrophages play crucial roles in atherosclerosis, we examined whether triglyceride-rich lipoproteins (TRLs), the major lipoproteins, in plasma of ApoCIIItg mice affect inflammation and ER stress levels in these cells. To further investigate the role of ApoCIII and triglyceride, we incubated HUVECs cells and peritoneal macrophages with TRLs with or without ApoCIII.
Results
Increased inflammation and ER stress were found in the aorta of ApoCIIItg mice. TRLs increased ER stress and oxidative stress in HUVECs and macrophages in a dose dependent. Moreover, TRLs together with ApoCIII could induce a higher inflammation level than TRLs alone in these cells.
Conclusions
Both TRLs and ApoCIII contribute to the progression of atherosclerosis, and the modulation of TRLs and ApoCIII may represent a novel therapeutic approach against HTG induced atherosclerosis.
Springer