Nicotinamide mononucleotide (NMN) mediates alleviation of poly(I:C) induced inflammatory response in human primary cell cultures
NMN is the direct precursor of the nicotinamide adenine dinucleotide (NAD+) and is considered a key component to increase NAD+ levels and mitochondrial activity in cells. In this study, based on transcriptome analysis, we showed that NMN alleviates poly(I:C)-induced inflammatory response in two types of human primary cell cultures, human pulmonary microvascular endothelial cells (HPMEC) and human coronary artery endothelial cells (HCAEC). The major inflammatory mediators including IL-6 and PARP family members are grouped into co-expressed gene modules and significantly down-regulated under NMN-dosage in poly(I:C)-induced conditions in both cell types. The Bayesian network analysis of module hub genes predicted common genes including eukaryotic translation initiation factor 1B (EIF1B) and distinct genes such as platelet-derived growth factor binding molecules in HCAEC, which potentially regulate the identified inflammation modules. These results have suggested the robust regulatory mechanism of NMN to alleviate inflammatory pathways, which may open up the possibility of a new role for NMN replenishment in chronic or acute inflammation treatment. Overall design: Comparative gene expression profiling analysis of RNA-seq data for HPMEC and HCAEC, with and without Poly(I:C) treatment and with three dosages of NM  N (0.1, 1, 10 mM), with matching controls.