Effect of n-alkanes on development of experimental atherosclerosis in rabbits

1973 ◽  
Vol 75 (1) ◽  
pp. 16-19
Author(s):  
A. A. Pokrovskii ◽  
L. G. Ponomareva ◽  
M. M. Levachev ◽  
A. L. Pozdnyakov ◽  
R. A. Pilenitsina
Keyword(s):  
Experimental Atherosclerosis

EXPERIMENTAL ATHEROSCLEROSIS WITH ASCORBIC ACID DEFICIENCY

1971 ◽  
Vol 35 (12) ◽  
pp. 1559-1565 ◽  
Author(s):  
TAKAO FUJITANI ◽  
KOTA OKADO ◽  
KATSUJI SENDA ◽  
MUNEAKI SUGIMURA ◽  
MOTOAKI KISHIKAWA
Keyword(s):  
Ascorbic Acid ◽  
Experimental Atherosclerosis ◽  
Ascorbic Acid Deficiency ◽  
Acid Deficiency

Studies in Experimental Atherosclerosis

1951 ◽  
Vol 6 (4) ◽  
pp. 358-364 ◽  
Author(s):  
O. J. Pollak ◽  
W. Bella
Keyword(s):  
Experimental Atherosclerosis

The Effect of Large Doses of Inositol On Experimental Atherosclerosis

Angiology ◽  
1952 ◽  
Vol 3 (3) ◽  
pp. 238-240 ◽  
Author(s):  
Campbell Moses ◽  
Grace L. Rhodes ◽  
Agatha Delacio
Keyword(s):  
Experimental Atherosclerosis

M.450 Isoflavone on experimental atherosclerosis in mice

2004 ◽  
Vol 5 (1) ◽  
pp. 104
Author(s):  
L. Asakura ◽  
P. Cazita ◽  
V. Sutti Nunes ◽  
L. Harada ◽  
J. Berti ◽  
...  
Keyword(s):  
Experimental Atherosclerosis

Abstract 48: Deletion of the Neuronal Guidance Molecule Epha2 Reduces Inflammation in Experimental Atherosclerosis

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Steven D Funk ◽  
Arif Yurdagul ◽  
Jonette Green ◽  
Patrick Albert ◽  
Marshall McInnis ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Activation ◽  
Experimental Atherosclerosis ◽  
Marker Genes ◽  
Endothelial Cell Activation ◽  
Enhanced Expression ◽  
Guidance Molecule ◽  
Neuronal Guidance ◽  
Deficient Mice

Neuronal guidance molecules are increasingly implicated in inflammatory responses. Recently, our group demonstrated enhanced expression of the neuronal guidance molecule EphA2 and its ephrinA1 ligand in mouse and human atherosclerotic plaques, and elucidated a novel proinflammatory function for EphA2 perpetuating proinflammatory gene expression during endothelial cell activation. However, a direct role for Eph/ephrins in atherosclerosis has never been demonstrated. We now show that knocking out the EphA2 gene in Western diet-fed ApoE mice blunts atherosclerotic plaque location at multiple sites. This reduction in atherosclerosis is associated with decreased monocyte infiltration and diminished expression of proinflammatory genes. EphA2 reduction may affect monocyte homing through multiple mechanisms, since reducing EphA2 expression in cytokine-activated endothelial cells does not affect endothelial adhesion molecule expression or monocyte rolling but significantly decreases firm adhesion in primary human monocytes. Like endothelial cells, plaque macrophages also express EphA2, and macrophages derived from EphA2 deficient mice show diminished expression of M1 marker genes and enhanced expression of M2 marker genes compared to their ApoE counterparts. Surprisingly, EphA2 deficient mice show significantly elevated plasma cholesterol. However, this elevation does not involve increased LDL levels but instead occurs due to elevations in plasma HDL levels. Taken together, the current data suggest EphA2 inhibition results in a multifaceted protective effect on experimental atherosclerosis characterized by reduced endothelial cell activation, monocyte recruitment, and M1/M2 polarization and enhanced circulating HDL levels.

REMODELING OF THE SMALL CALIBER CORONARY VESSELS IN EXPERIMENTAL ATHEROSCLEROSIS

2021 ◽  
Vol 17 (75) ◽  
pp. 225
Author(s):  
N. S. Tryasak ◽  
Yu. V. Silkina ◽  
G. A. Klopotskіy ◽  
A. E. Khudyakov
Keyword(s):  
Coronary Vessels ◽  
Experimental Atherosclerosis
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