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首页> 外文期刊>Circulation journal >Endogenous Interleukin-1β Is Implicated in Intraplaque Hemorrhage in Apolipoprotein E Gene Null Mice
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Endogenous Interleukin-1β Is Implicated in Intraplaque Hemorrhage in Apolipoprotein E Gene Null Mice

机译：内源性白细胞介素1β参与载脂蛋白E基因空小鼠的斑块内出血

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Background: Intraplaque hemorrhage (IPH) has been implicated in plaque instability and rupture in atherosclerotic lesions, although the mechanisms by which IPH progresses remain largely unknown. In this study, apolipoprotein E-deficient mice with carotid artery ligation and cuff placement around the artery were used, and pro-inflammatory cytokines that are implicated in IPH were analyzed. Methods?and?Results: The expression of interleukin-1β (IL-1β) increased significantly following cuff placement compared with mice with carotid artery ligation alone. IPH occurred in the cuff-placed carotid artery following treatment with the negative control (NC) small interfering RNA (siRNA). However, the occurrence was significantly reduced in the cuff-placed carotid artery following treatment with an IL-1β siRNA. Neovessel formation was significantly reduced in the carotid artery treated with the NC siRNA compared with that treated with IL-1β siRNA. IL-1β significantly inhibited the tube formation and wound healing capacities of vascular endothelial cells in vitro. Furthermore, immunostaining of matrix metalloproteinase-9 (MMP-9) significantly increased in the carotid artery treated with the NC siRNA compared with that treated with IL-1β siRNA. Conclusions: These results suggest that endogenous IL-1β is implicated in the progression of IPH via the inhibition of physiological angiogenesis in the atherosclerotic plaque, leading to the formation of leaky neovessels. Furthermore, the stimulation of MMP-9 expression may also contribute to the formation of leaky neovessels.
机译：背景：斑块内出血（IPH）与动脉粥样硬化病变的斑块不稳定性和破裂有关，尽管IPH进展的机制仍不清楚。在这项研究中，使用载脂蛋白E缺陷型小鼠的颈动脉结扎并在动脉周围放置袖带，并分析了与IPH有关的促炎性细胞因子。方法和结果：与单独进行颈动脉结扎的小鼠相比，袖套放置后白细胞介素-1β（IL-1β）的表达显着增加。经阴性对照（NC）小干扰RNA（siRNA）处理后，IPH发生在放置于袖带的颈动脉中。但是，在用IL-1βsiRNA治疗后，置入袖带的颈动脉的发生率显着降低。与用IL-1βsiRNA处理的颈动脉相比，用NC siRNA处理的颈动脉新血管形成明显减少。 IL-1β在体外显着抑制血管内皮细胞的管形成和伤口愈合能力。此外，与IL-1βsiRNA处理相比，NC siRNA处理的颈动脉中基质金属蛋白酶9（MMP-9）的免疫染色显着增加。结论：这些结果表明，内源性IL-1β通过抑制动脉粥样硬化斑块中的生理性血管生成而参与IPH的进展，从而导致渗漏的新血管的形成。此外，MMP-9表达的刺激也可能有助于形成渗漏的新血管。

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