Complement protein C1q modulates macrophage molecular signaling and inflammatory responses during ingestion of atherogenic lipoproteins. Homo sapiens

C1q suppresses JAK-STAT signal transduction and activates PPAR-mediated transcription in macrophages during clearance of modified forms of LDL leading to a reduction in inflammatory response. Overall design: Human monocyte-derived macrophages (HMDM) were incubated with either oxidized (oxLDL) or acetylated low-density lipoprotein (acLDL) in the presence or absence of C1q for 3 hours. Total RNA was extracted using the Qiagen RNeasy Mini Kit. RNA libraries were constructed using the Illumina TruSeq Stranded mRNA Sample Preparation Kit. Sequences were aligned to a reference genome (hg38), RPKM and raw counts were determined using CASAVA version 1.8.2.

C1q在巨噬细胞清除修饰型低密度脂蛋白（modified LDL）的过程中，可抑制JAK-STAT信号转导（JAK-STAT signal transduction）并激活过氧化物酶体增殖物激活受体（PPAR）介导的转录，从而减轻炎症反应。实验设计：将人单核细胞源性巨噬细胞（HMDM）分别与氧化型低密度脂蛋白（oxLDL）或乙酰化低密度脂蛋白（acLDL）孵育，同时设置添加C1q与不添加C1q的组别，孵育时长为3小时。随后采用Qiagen RNeasy Mini试剂盒提取总RNA，使用Illumina TruSeq Stranded mRNA样本制备试剂盒构建RNA文库。将测序序列比对至参考基因组hg38，并通过CASAVA 1.8.2版本计算每百万reads每千碱基片段数（RPKM）与原始计数。