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首页> 外文期刊>Cytokine >Overexpression of CXCL16 promotes a vulnerable plaque phenotype in Apolipoprotein E-Knockout Mice.
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Overexpression of CXCL16 promotes a vulnerable plaque phenotype in Apolipoprotein E-Knockout Mice.

机译：CXCL16的过度表达促进载脂蛋白E基因敲除小鼠中的易损斑块表型。

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BACKGROUND: CXCL16 has been shown to be involved in atherosclerotic lesion development, but its role in preexisting lesions is still unclear. This study aims to assess the effect of CXCL16 on the stability of preexisting lesions. METHODS: We firstly measured plasma CXCL16 level in Apolipoprotein E-Knockout (ApoE KO) mice with either high-cholesterol diet (HCD) or normal diet (ND) by enzyme-linked immunosorbent assay (ELISA). Then, silastic collars were placed around the carotid arteries in HCD-ApoE KO mice to accelerate atherosclerotic lesions. Five weeks later, CXCL16 was overexpressed by intravenous injection of lentivirus carrying CXCL16 transgene. Two weeks after infection, lesions were stained with hematoxylin and eosin (HE) and with oil red O. Biomarkers in the lesions, such as MMPs, CCL2, VCAM-1 and TNF-alpha were measured by real-time polymerase chain reaction (RT-PCR), which indicate the instability of plaques. RESULTS: The level of CXCL16 in plasma was higher in HCD-ApoE KO mice as compared to ND-ApoE KO mice. Circulating CXCL16 overexpression does not affect the size of preexisting plaques, but it leads to vulnerable plaque morphology and increases the expression of markers of plaque destabilization. CONCLUSION: Systemic CXCL16 becomes much higher in atherosclerosis, and it could be a potential atherogenic biomarker. Overexpression of CXCL16 promotes the evolution of preexisting lesions to vulnerable plaques in ApoE KO mice.
机译：背景：CXCL16已被证明参与动脉粥样硬化病变的发展，但其在已有病变中的作用仍不清楚。这项研究旨在评估CXCL16对既有病变稳定性的影响。方法：我们首先通过酶联免疫吸附试验（ELISA）测定了高胆固醇饮食（HCD）或正常饮食（ND）的载脂蛋白E基因敲除（ApoE KO）小鼠的血浆CXCL16水平。然后，在HCD-ApoE KO小鼠的颈动脉周围放置硅橡胶项圈，以加速动脉粥样硬化病变。五周后，通过静脉注射携带CXCL16转基因的慢病毒，CXCL16过表达。感染两周后，用苏木精和曙红（HE）以及油红色O对病变进行染色。通过实时聚合酶链反应（RT）测量病变中的生物标志物，如MMPs，CCL2，VCAM-1和TNF-alpha -PCR），表明斑块不稳定。结果：与ND-ApoE KO小鼠相比，HCD-ApoE KO小鼠的血浆CXCL16水平更高。循环的CXCL16过表达不会影响预先存在的噬斑的大小，但会导致脆弱的噬斑形态并增加噬斑去稳定化标记的表达。结论：全身性CXCL16在动脉粥样硬化中变得更高，并且可能是潜在的动脉粥样硬化生物标志物。 CXCL16的过表达促进ApoE KO小鼠中先前存在的病变向易损斑块的演变。

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