ATTENUATED FREE CHOLESTEROL LOADING-INDUCED APOPTOSIS BUT PRESERVED PHOSPHLIPID

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 以往的研究表明，磷脂酶A(2)组(iPLA2β)参与了内质网应激诱导的细胞凋亡，小鼠巨噬细胞在自由胆固醇负荷(FCL)时经历内质网应激和细胞凋亡。我们最近培育了ipla(2)β缺失的小鼠，在这里我们证明了ipla(2)β缺失的巨噬细胞降低了对FCL诱导的凋亡的敏感性，尽管它们和野生型(WT)细胞在转录调节因子CHOP方面表现出类似的增加。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Previous studies suggest that Group VIA Phospholipase A(2) (iPLA(2)beta) participates in ER-stress induced apoptosis, and mouse macrophages undergo ER stress and apoptosis upon free cholesterol loading (FCL). We recently generated iPLA(2)beta-null mice, and here we demonstrate that iPLA(2)beta-null macrophages have reduced sensitivity to FCL-induced apoptosis, although they and wild-type (WT) cells exhibit similar increases in the transcriptional regulator CHOP.