氧化型低密度脂蛋白诱导巨噬细胞中 caspase-1 介导的细胞焦亡：对病变不稳定性的影响？

Oxidized low density lipoprotein induced caspase-1 mediated pyroptotic cell death in macrophages: implication in lesion instability?

机构信息

Department of Cardiovascular Medicine, Shaanxi Provincial People's Hospital, Xi'an, China.

出版信息

PLoS One. 2013 Apr 25;8(4):e62148. doi: 10.1371/journal.pone.0062148. Print 2013.

BACKGROUND

Macrophage death in advanced lesion has been confirmed to play an important role in plaque instability. However, the mechanism underlying lesion macrophage death still remains largely unknown.

METHODS AND RESULTS

Immunohistochemistry showed that caspase-1 activated in advanced lesion and co-located with macrophages and TUNEL positive reaction. In in-vitro experiments showed that ox-LDL induced caspase-1 activation and this activation was required for ox-LDL induced macrophages lysis, IL-1β and IL-18 production as well as DNA fragmentation. Mechanism experiments showed that CD36 and NLRP3/caspase-1/pathway involved in ox-LDL induced macrophage pyroptosis.

CONCLUSION

Our study here identified a novel cell death, pyroptosis in ox-LDL induced human macrophage, which may be implicated in lesion macrophages death and play an important role in lesion instability.

背景

晚期病变中巨噬细胞的死亡被证实对斑块不稳定起着重要作用。然而，病变中巨噬细胞死亡的机制在很大程度上仍然未知。

方法和结果

免疫组化显示，caspase-1 在晚期病变中被激活，与巨噬细胞共定位，并与 TUNEL 阳性反应。在体外实验中，ox-LDL 诱导 caspase-1 激活，这种激活对于 ox-LDL 诱导的巨噬细胞裂解、IL-1β 和 IL-18 的产生以及 DNA 片段化是必需的。机制实验表明，CD36 和 NLRP3/caspase-1/途径参与了 ox-LDL 诱导的巨噬细胞细胞焦亡。