scholarly journals Omentin attenuates atherosclerotic lesion formation in apolipoprotein E-deficient mice

2015 ◽  
Vol 110 (1) ◽  
pp. 107-117 ◽  
Author(s):  
Mizuho Hiramatsu-Ito ◽  
Rei Shibata ◽  
Koji Ohashi ◽  
Yusuke Uemura ◽  
Noriyoshi Kanemura ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
Atherosclerotic Lesion ◽  
Lesion Formation ◽  
Deficient Mice ◽  
Atherosclerotic Lesion Formation

scholarly journals The Endogenous Estradiol Metabolite 2-Methoxyestradiol Reduces Atherosclerotic Lesion Formation in Female Apolipoprotein E-Deficient Mice

Endocrinology ◽  
2007 ◽  
Vol 148 (9) ◽  
pp. 4128-4132 ◽  
Author(s):  
Johan Bourghardt ◽  
Göran Bergström ◽  
Alexandra Krettek ◽  
Sara Sjöberg ◽  
Jan Borén ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
Low Dose ◽  
Hormone Replacement ◽  
Atherosclerotic Lesion ◽  
Total Serum ◽  
High Dose ◽  
Lesion Formation ◽  
Cholesterol Levels ◽  
Deficient Mice ◽  
Atherosclerotic Lesion Formation

Estradiol, the major endogenous estrogen, reduces experimental atherosclerosis and metabolizes to 2-methoxyestradiol in vascular cells. Currently undergoing evaluation in clinical cancer trials, 2-methoxyestradiol potently inhibits cell proliferation independently of the classical estrogen receptors. This study examined whether 2-methoxyestradiol affects atherosclerosis development in female mice. Apolipoprotein E-deficient mice, a well-established mouse model of atherosclerosis, were ovariectomized and treated through slow-release pellets with placebo, 17β-estradiol (6 μg/d), or 2-methoxyestradiol [6.66 μg/d (low-dose) or 66.6 μg/d (high-dose)]. After 90 d, body weight gain decreased and uterine weight increased in the high-dose but not low-dose 2-methoxyestradiol group. En face analysis showed that the fractional area of the aorta covered by atherosclerotic lesions decreased in the high-dose 2-methoxyestradiol (52%) but not in the low-dose 2-methoxyestradiol group. Total serum cholesterol levels decreased in the high- and low-dose 2-methoxyestradiol groups (19%, P < 0.05 and 21%, P = 0.062, respectively). Estradiol treatment reduced the fractional atherosclerotic lesion area (85%) and decreased cholesterol levels (42%). In conclusion, our study shows for the first time that 2-methoxyestradiol reduces atherosclerotic lesion formation in vivo. The antiatherogenic activity of an estradiol metabolite lacking estrogen receptor activating capacity may argue that trials on cardiovascular effects of hormone replacement therapy should use estradiol rather than other estrogens. Future research should define the role of 2-methoxyestradiol as a mediator of the antiatherosclerotic actions of estradiol. Furthermore, evaluation of the effects of 2-methoxyestradiol on cardiovascular disease endpoints in ongoing clinical trials is of great interest.

scholarly journals Effect of Dalteparin on Atherosclerotic Lesion Formation in Apolipoprotein E-Deficient Mice

2013 ◽  
Vol 21 (3) ◽  
pp. 266-272
Author(s):  
Lin Su ◽  
Qingwen Zhang ◽  
Hui Bao ◽  
Wei Li ◽  
Yide Miao ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
Atherosclerotic Lesion ◽  
Lesion Formation ◽  
Deficient Mice ◽  
Atherosclerotic Lesion Formation

Disodium ascorbyl phytostanyl phosphate reduces plasma cholesterol concentrations and atherosclerotic lesion formation in apolipoprotein E-deficient mice

Metabolism ◽  
2003 ◽  
Vol 52 (4) ◽  
pp. 425-431 ◽  
Author(s):  
Tatjana Lukic ◽  
Kishor M. Wasan ◽  
Daniela Zamfir ◽  
Mohammed H. Moghadasian ◽  
P.Haydn Pritchard
Keyword(s):  
Apolipoprotein E ◽  
Plasma Cholesterol ◽  
Atherosclerotic Lesion ◽  
Lesion Formation ◽  
Deficient Mice ◽  
Atherosclerotic Lesion Formation

Lack of vitamin d receptor accelerates atherosclerotic lesion formation in apolipoprotein E-deficient mice

2014 ◽  
Vol 235 (2) ◽  
pp. e28
Author(s):  
M. Bozic ◽  
M. Ibarz ◽  
J.F. Navarro-Gonzalez ◽  
M.D. Sanchez-Niño ◽  
A. Ortiz ◽  
...  
Keyword(s):  
Vitamin D ◽  
Apolipoprotein E ◽  
Vitamin D Receptor ◽  
Atherosclerotic Lesion ◽  
Lesion Formation ◽  
Deficient Mice ◽  
Atherosclerotic Lesion Formation

Abstract 83: Bone Marrow Derived Cells Do Not Mediate Reductions in Cholesterol, Atherosclerosis and Adiposity in Microsomal Prostaglindin E Synthase 1 Deficient Mice Fed High Fat Diets Enriched in Cholesterol

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Sarah Srodulski ◽  
Victoria L King
Keyword(s):  
Bone Marrow ◽  
Weight Gain ◽  
Marrow Cell ◽  
Atherosclerotic Lesion ◽  
Chimeric Mice ◽  
High Fat ◽  
Lesion Formation ◽  
Bone Marrow Derived Cells ◽  
Deficient Mice ◽  
Atherosclerotic Lesion Formation

Microsomal prostaglandin E 2 synthase-1 (mPGES-1) catalyzes the conversion of COX-2 generated PGH 2 to PGE 2 and is the predominate source of PGE 2 during and inflammatory response. We and others have demonstrated that mPGES-1 deficiency attenuates atherosclerosis in mice on a mixed background. The present study investigated the effect of mPGES-1 deficiency on atherosclerosis in C57BL/6 low density lipoprotein receptor deficient (LDLr-/-) mice. mPGES-1 deficiency attenuated atherosclerosis in LDLr-/- mice fed either a low fat (LF) (P = 0.02) or high fat (HF) (P = 0.0026) diet enriched with cholesterol, or a western diet (P = 0.02) for 17 weeks. mPGES-1 deficiency attenuated weight gain and cholesterol concentrations in mice fed a western (P = 0.004 and P < 0.05; respectively) or HF diet (P = 0.01 and P = 0.012, respectively). However, body weight and cholesterol concentrations were not different in mice fed the LF diet. These data suggest that different mechanisms mediate the reduction in atherosclerosis in mPGES-1 deficient mice fed LF and HF diets. To determine if mPGES-1 deficiency in macrophages contributed to the reduction in atherosclerosis in mice fed HF diets, 4 groups of chimeric mice were generated. Four weeks post bone marrow cell transplant (BMT) mice were fed a western diet. BMT attenuated weight gain in all groups of chimeric mice; however, weight gain was not different between any of the groups. BMT decreased atherosclerotic lesion formation 10 fold in all groups of mice. Neither bone marrow cell specific deficiency of mPGES-1 (KO>WT) or mPGES-1 specific expression in bone marrow derived cells (WT>KO) had an effect on lesion formation compared to WT>WT or KO>KO mice. Cholesterol concentrations were decreased in KO>KO and WT>KO mice compared to WT>WT (P < 0.01) and KO>WT (P< 0.05) mice. These data suggest that mPGES-1 expression in bone marrow derived cells does not contribute to the development of atherosclerosis. Moreover, these data suggest that prostanoids may play a role in hepatic cholesterol homeostasis in mice fed HF diets enriched in cholesterol thereby contributing to atherosclerotic lesion formation. Moreover, these data provide further evidence that prostanoids play a role in regulating the accumulation of diet-induced adiposity.

scholarly journals 14Hematopoietic complement factor H deficiency elevates plasma IgM levels and reduces atherosclerotic lesion formation in Ldlr deficient mice

2018 ◽  
Vol 114 (suppl_1) ◽  
pp. S3-S3
Author(s):  
M Kiss ◽  
D Tsiantoulas ◽  
N Papac-Milicevic ◽  
L Goderle ◽  
M Ozsvar-Kozma ◽  
...  
Keyword(s):  
Atherosclerotic Lesion ◽  
Factor H ◽  
Complement Factor H ◽  
Complement Factor ◽  
Lesion Formation ◽  
Factor H Deficiency ◽  
Deficient Mice ◽  
Atherosclerotic Lesion Formation

scholarly journals Effect of MMP-2 Deficiency on Atherosclerotic Lesion Formation in ApoE-Deficient Mice

2006 ◽  
Vol 26 (5) ◽  
pp. 1120-1125 ◽  
Author(s):  
Masafumi Kuzuya ◽  
Kae Nakamura ◽  
Takeshi Sasaki ◽  
Xian Wu Cheng ◽  
Shigeyoshi Itohara ◽  
...  
Keyword(s):  
Atherosclerotic Lesion ◽  
Lesion Formation ◽  
Deficient Mice ◽  
Atherosclerotic Lesion Formation
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