Department of Pain and Translational Symptom Science, School of Nursing, University of Maryland, Baltimore, Maryland, USA.
Department of Anesthesiology and Psychiatry, School of Medicine, University of Maryland, Baltimore, Maryland, USA.
Clin Pharmacol Ther. 2024 Aug;116(2):380-389. doi: 10.1002/cpt.3286. Epub 2024 May 6.
Gene expression networks associated with placebo effects are understudied; in this study, we identified transcriptomic profiles associated with placebo responsivity. Participants suffering from chronic pain underwent a verbal suggestion and conditioning paradigm with individually tailored thermal painful stimulations to elicit conditioned placebo effects. Participants reported pain intensity on a visual analog scale (VAS) anchored from zero = no pain to 100 = maximum imaginable pain. RNA was extracted from venous blood and RNA sequencing and validation tests were performed to identify differentially expressed genes (DEGs) associated with placebo effects, controlling for sex and level of pain. Unbiased enrichment analyses were performed to identify biological processes associated with placebo effects. Of the 10,700 protein-coding genes that passed quality control filters, 667 were found to be associated with placebo effects (FDR <0.05). Most genes (97%) upregulated were associated with larger placebo effects. The 17 top transcriptome-wide significant genes were further validated via RT-qPCR in an independent cohort of chronic pain participants. Six of them (CCDC85B, FBXL15, HAGH, PI3, SELENOM, and TNFRSF4) showed positive and significant (P < 0.05) correlation with placebo effects in the cohort. The overall DEGs were highly enriched in regulation of expression of SLITs and ROBOs (R-HSA-9010553, FDR = 1.26e-33), metabolism of RNA (R-HSA-8953854, FDR = 1.34e-30), Huntington's disease (hsa05016, FDR = 9.84e-31), and ribosome biogenesis (GO:0042254, FDR = 2.67e-15); alternations in these pathways might jeopardize the proneness to elicit placebo effects. Future studies are needed to replicate this finding and better understand the unique molecular dynamics of people who are more or less affected by pain and placebo.
与安慰剂效应相关的基因表达网络研究较少;在这项研究中,我们确定了与安慰剂反应性相关的转录组谱。患有慢性疼痛的参与者接受了口头暗示和条件作用范式,并用个体化定制的热痛刺激来引起条件性安慰剂效应。参与者使用视觉模拟量表(VAS)报告疼痛强度,范围从 0=无疼痛到 100=最大可想象疼痛。从静脉血中提取 RNA,并进行 RNA 测序和验证测试,以鉴定与安慰剂效应相关的差异表达基因(DEGs),同时控制性别和疼痛水平。进行无偏富集分析以鉴定与安慰剂效应相关的生物学过程。在通过质量控制过滤的 10700 个蛋白质编码基因中,有 667 个与安慰剂效应相关(FDR<0.05)。上调的大多数基因(97%)与更大的安慰剂效应相关。进一步在独立的慢性疼痛参与者队列中通过 RT-qPCR 验证了 17 个转录组全显著基因。其中 6 个基因(CCDC85B、FBXL15、HAGH、PI3、SELENOM 和 TNFRSF4)在队列中与安慰剂效应呈正相关且具有统计学意义(P<0.05)。总体 DEGs 在 SLITs 和 ROBOs 的表达调控(R-HSA-9010553,FDR=1.26e-33)、RNA 代谢(R-HSA-8953854,FDR=1.34e-30)、亨廷顿病(hsa05016,FDR=9.84e-31)和核糖体生物发生(GO:0042254,FDR=2.67e-15)中高度富集;这些途径的改变可能会危及诱发安慰剂效应的倾向。需要进一步的研究来复制这一发现,并更好地理解对疼痛和安慰剂的影响程度不同的人的独特分子动力学。