scholarly journals Cryptotanshinone, an orally bioactive herbal compound from Danshen, attenuates atherosclerosis in apolipoprotein E-deficient mice: role of lectin-like oxidized LDL receptor-1 (LOX-1)

2015 ◽  
Vol 172 (23) ◽  
pp. 5661-5675 ◽  
Author(s):  
Zhiping Liu ◽  
Suowen Xu ◽  
Xiaoyang Huang ◽  
Jiaojiao Wang ◽  
Si Gao ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
Oxidized Ldl ◽  
Ldl Receptor ◽  
Herbal Compound ◽  
Deficient Mice

F(ab′)2 fragments of anti-oxidized LDL IgG attenuate vascular inflammation and atherogenesis in diabetic LDL receptor-deficient mice

2016 ◽  
Vol 173 ◽  
pp. 50-56 ◽  
Author(s):  
Yanchun Li ◽  
Zhongyang Lu ◽  
Yan Huang ◽  
Maria F. Lopes-Virella ◽  
Gabriel Virella
Keyword(s):  
Oxidized Ldl ◽  
Vascular Inflammation ◽  
Ldl Receptor ◽  
Deficient Mice

scholarly journals Oxidized LDL but not angiotensin II induces the interaction between LOX-1 and AT1 receptors

2020 ◽  
Author(s):  
Li Lin ◽  
Ning Zhou ◽  
Le Kang ◽  
Qi Wang ◽  
Jian Wu ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Oxidized Ldl ◽  
Low Density Lipoprotein ◽  
Ldl Receptor ◽  
Density Lipoprotein ◽  
Direct Interaction ◽  
Cardiomyocyte Hypertrophy ◽  
Oxidized Low Density Lipoprotein ◽  
Protein Activation

Oxidized low-density lipoprotein (Ox-LDL) can induce cardiac hypertrophy, but the mechanism is still unclear. Here we elucidate the role of angiotensin II (AngII) receptor (AT1-R) in Ox-LDL-induced cardiomycyte hypertrophy. Inhibition of Ox-LDL receptor LOX-1 and AT1-R rather than AngII abolished Ox-LDL-induced hypertrophic responses. Similar results were obtained from the heart of mice lacking endogenous Ang II and their cardiomyocytes. Ox-LDL but not AngII induced binding of LOX-1 to AT1-R, and the inhibition of LOX-1 or AT1-R rather than AngII abolished the association of these two receptors. Ox-LDL-induced ERKs phosphorylation in LOX-1 and AT1-R-overexpression cells and the binding of both receptors were suppressed by the mutants of LOX-1 (Lys266Ala/Lys267Ala) or AT1-R (Glu257Ala), however, the AT1-R mutant lacking Gq protein-coupling ability only abolished the ERKs phosphorylation. The phosphorylation of ERKs induced by Ox-LDL in LOX-1 and AT1-R-overexpression cells was abrogated by Gq protein inhibitor but not by Jak2, Rac1 and RhoA inhibitors. Therefore, the direct interaction between LOX-1 and AT1-R and the downstream Gq protein activation are important mechanisms for Ox-LDL- but not AngII-induced cardiomyocyte hypertrophy

scholarly journals Chronic iron overload intensifies atherosclerosis in apolipoprotein E deficient mice: Role of oxidative stress and endothelial dysfunction

Life Sciences ◽  
2019 ◽  
Vol 233 ◽  
pp. 116702 ◽  
Author(s):  
Vinícius Bermond Marques ◽  
Marcos André Soares Leal ◽  
Jandinay Gonzaga Alexandre Mageski ◽  
Helbert Gabriel Fidelis ◽  
Breno Valentim Nogueira ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Iron Overload ◽  
Apolipoprotein E ◽  
Deficient Mice

scholarly journals Role of Interleukin 17A in Aortic Valve Inflammation in Apolipoprotein E-deficient Mice

2020 ◽  
Vol 40 (4) ◽  
pp. 729-738
Author(s):  
Fa-yuan Liu ◽  
Peng Bai ◽  
Ye-fan Jiang ◽  
Nian-guo Dong ◽  
Geng Li ◽  
...  
Keyword(s):  
Aortic Valve ◽  
Apolipoprotein E ◽  
Interleukin 17A ◽  
Deficient Mice
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