Adiponectin reduces atherosclerosis in apolipoprotein E-deficient mice
Adiponectin reduces atherosclerosis in apolipoprotein E-deficient mice
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DOI：
10.1161/01.cir.0000042707.50032.19
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发表时间：
2002-11-26
期刊：
影响因子：
37.8
通讯作者：
Matsuzawa, Y
中科院分区：
文献类型：
--
作者：
Okamoto, Y;Kihara, S;Matsuzawa, Y
背景：脂肪细胞来源的生物活性分子的调节失调在动脉粥样硬化的发展中起着重要作用。我们先前报道，脂联素是一种脂肪细胞特异的血浆蛋白，在体外可从血浆蓄积在损伤的动脉中，抑制内皮炎性反应和血管平滑肌细胞的增殖，以及巨噬细胞向泡沫细胞的转化。本研究探讨了血浆脂联素的升高是否真的能在活体内减少动脉粥样硬化。方法和结果：用表达人脂联素的重组腺病毒(Ad-APN)或β-半乳糖苷酶(Ad-Betagal)治疗载脂蛋白E缺陷小鼠。Ad-APN组小鼠的血浆脂联素水平是Ad-Betagal组的48倍。注射后第14天，Ad-APN组小鼠主动脉窦病变的形成比Ad-Betagal组小鼠抑制了30%(P
Background-Dysregulation of adipocyte-derived bioactive molecules plays an important role in the development of atherosclerosis., We previously reported that adiponectin, an adipocyte-specific plasma protein, accumulated in the injured artery from the plasma and suppressed endothelial inflammatory response and vascular smooth muscle cell proliferation, as well as macrophage-to-foam cell transformation in vitro. The current study investigated whether the increased plasma adiponectin could actually reduce atherosclerosis in vivo.Methods and Results-Apolipoprotein E-deficient mice were treated with recombinant adenovirus expressing human adiponectin (Ad-APN) or beta-galactosidase (Ad-betagal). The plasma adiponectin levels in Ad-APN-treated mice increased 48 times as much as those in Ad-betagal treated mice. On the 14th day after injection, the lesion formation in aortic sinus was inhibited in Ad-APN-treated mice by 30% compared with Ad-betagal-treated mice (P