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Merck
  • Disruption of p21-activated kinase 1 gene diminishes atherosclerosis in apolipoprotein E-deficient mice.

Disruption of p21-activated kinase 1 gene diminishes atherosclerosis in apolipoprotein E-deficient mice.

Nature communications (2015-06-25)
Nikhlesh K Singh, Sivareddy Kotla, Elena Dyukova, James G Traylor, A Wayne Orr, Jonathan Chernoff, Tony N Marion, Gadiparthi N Rao
摘要

Pak1 plays an important role in various cellular processes, including cell motility, polarity, survival and proliferation. To date, its role in atherogenesis has not been explored. Here we report the effect of Pak1 on atherogenesis using atherosclerosis-prone apolipoprotein E-deficient (ApoE(-/-)) mice as a model. Disruption of Pak1 in ApoE(-/-) mice results in reduced plaque burden, significantly attenuates circulating IL-6 and MCP-1 levels, limits the expression of adhesion molecules and diminishes the macrophage content in the aortic root of ApoE(-/-) mice. We also observed reduced oxidized LDL uptake and increased cholesterol efflux by macrophages and smooth muscle cells of ApoE(-/-):Pak1(-/-) mice as compared with ApoE(-/-) mice. In addition, we detect increased Pak1 phosphorylation in human atherosclerotic arteries, suggesting its role in human atherogenesis. Altogether, these results identify Pak1 as an important factor in the initiation and progression of atherogenesis.

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Sigma-Aldrich
胆固醇, Sigma Grade, ≥99%
Sigma-Aldrich
单克隆抗-肌动蛋白,α-平滑肌, clone 1A4, ascites fluid
Sigma-Aldrich
胶原酶 来源于溶组织梭菌, Type XI, 2-5 FALGPA units/mg solid, ≥800 CDU/mg solid