Supplementing NMN to Protect Osteoblasts Against LPS-Induced Inflammation
Introduction
It has been reported that infection with Gram-negative bacteria can disrupt the osteogenic differentiation. Notably, nicotinamide mononucleotide (NMN) protects against osteogenesis from inflammation caused by Gram-negative bacterial infections possibly via regulating the Wnt/β-catenin signaling pathway.
About osteogenic differentiation
Osteogenic differentiation refers to the formation process of osteoblasts from bone marrow mesenchymal stem/stromal (a.k.a. skeletal stem) cells and bone progenitor cells, which is a key event in bone formation during development, fracture repair, and tissue maintenance. Abnormalities in the process of osteogenic differentiation may disrupt physiological bone homeostasis, which is strongly associated with a variety of bone-related diseases such as osteoporosis, bone tumors, and osteoarthritis, making negative impacts upon fracture healing and repair of bone tissue defects.
LPS-induced suppression of osteogenesis
Lipopolysaccharide (LPS) is a component of the cell wall in Gram-negative bacteria, which is intensively applied to mimic Gram-negative bacterial infections in cell and animal models. LPS can hamper osteogenic differentiation of pre-osteoblasts MC3T3-E1 by diminishing the expression of mRNA markers (Alp1, Bglap, Runx2, and Sp7), ALP activity, and mineralization.
Partial protection of NMN against the LPS-induced suppression of osteogenesis
LPS-induced inhibition of osteogenic differentiation in MC3T3-E1 cells is partially offset by 1 mM of NMN. Concretely, the mRNA levels of Alp1, Bglap, and Sp7 in cells co-treated with NMN and LPS are relatively higher than those in cells treated solely with LPS. Furthermore, ALP activity and mineralization repressed by LPS are restored in the presence of NMN (1 mM).
Potential involvement of the Wnt/β-catenin signaling pathway in NMN's effect on osteogenesis
Wnt/β-catenin signaling pathway has been attested to play a vital role in osteogenesis by promoting bone formation and inhibiting bone resorption. In cells treated with LPS, β-catenin is localized in the cytoplasm rather than the nucleus. Following NMN treatment, β-catenin is translocated to the nucleus, similar to what occurred in response to the treatment of osteogenic induction medium (OIM). Meanwhile, the fluorescence intensity of β-catenin is restored upon NMN treatment.
Conclusion
NMN has a protective role against LPS-induced osteogenesis disruption, which is potentially achieved by the Wnt/β-catenin signaling pathway. NMN may function as a viable therapeutic strategy to preserve bone homeostasis in elderly and immunocompromised patients.
Reference
Kang I, Koo M, Jun JH, Lee J. Effect of nicotinamide mononucleotide on osteogenesis in MC3T3-E1 cells against inflammation-induced by lipopolysaccharide. Clin Exp Reprod Med. Published online April 11, 2024. doi:10.5653/cerm.2023.06744
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