Nicotinamide mononucleotide (NMN) alleviates the poly(I:C)-induced inflammatory response in human primary cell cultures

NMN is the direct precursor of nicotinamide adenine dinucleotide (NAD+) and is considered as a key factor for increasing NAD+ levels and mitochondrial activity in cells. In this study, based on transcriptome analysis, we showed that NMN alleviates the poly(I:C)-induced inflammatory response in cultu...

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Published in:Scientific reports 2023-07, Vol.13 (1), p.11765-11765, Article 11765
Main Authors: Sano, Hitomi, Kratz, Anton, Nishino, Taiko, Imamura, Haruna, Yoshida, Yuki, Shimizu, Noriaki, Kitano, Hiroaki, Yachie, Ayako
Format: Article
Language:English
Subjects:
631/114
631/553/2711
631/553/2714
Bayes Theorem
Bayesian analysis
Cell culture
Coronary artery
Coronary vessels
Endothelial cells
Endothelial Cells - metabolism
Gene expression
Growth factors
Humanities and Social Sciences
Humans
Inflammation
Inflammation - genetics
Laboratories
Metabolism
Microvasculature
multidisciplinary
NAD
NAD - metabolism
Nicotinamide Mononucleotide - pharmacology
Platelet-derived growth factor
Polyinosinic:polycytidylic acid
Primary Cell Culture
Science
Science (multidisciplinary)
Severe acute respiratory syndrome coronavirus 2
Transcription factors
Transcriptomes
Veins & arteries
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Summary:NMN is the direct precursor of nicotinamide adenine dinucleotide (NAD+) and is considered as a key factor for increasing NAD+ levels and mitochondrial activity in cells. In this study, based on transcriptome analysis, we showed that NMN alleviates the poly(I:C)-induced inflammatory response in cultures of two types of human primary cells, human pulmonary microvascular endothelial cells (HPMECs) and human coronary artery endothelial cells (HCAECs). Major inflammatory mediators, including IL6 and PARP family members, were grouped into coexpressed gene modules and significantly downregulated under NMN exposure in poly(I:C)-activated conditions in both cell types. The Bayesian network analysis of module hub genes predicted common genes, including eukaryotic translation initiation factor 4B ( EIF4B ), and distinct genes, such as platelet-derived growth factor binding molecules, in HCAECs, which potentially regulate the identified inflammation modules. These results suggest a robust regulatory mechanism by which NMN alleviates inflammatory pathway activation, which may open up the possibility of a new role for NMN replenishment in the treatment of chronic or acute inflammation.
ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-023-38762-x