Large changes in NAD levels associated with CD38 expression during HL-60 cell differentiation

Al-Abady, Zainab N.; Durante, Barbara; Moody, A. John; Billington, Richard

doi:10.1016/j.bbrc.2013.10.170

Cited by 9 publications

(7 citation statements)

References 29 publications

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“…This may reflect greater turnover of NAD + in these cells or that the increase in CD38 is related to its receptor functions. CD38 is unusual in that it can act as both a cell surface receptor (binding to adhesion molecule-1, CD31) and as an enzyme [ 29 ] but our knowledge of how exactly the two functions interact is scant [ 30 ]. CD38 is known to be a marker of classically activated (M1-like) macrophages [ 31 ] and our results suggest that CD38 might contribute to differentiated macrophage responses.…”

Section: Discussionmentioning

confidence: 99%

Intracellular NAD+ levels are associated with LPS-induced TNF-α release in pro-inflammatory macrophages

et al. 2016

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Section: Discussionmentioning

confidence: 99%

Intracellular NAD+ levels are associated with LPS-induced TNF-α release in pro-inflammatory macrophages

et al. 2016

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“…Studies also found that C3G is an inhibitor of CD38 and competitively inhibits the function of CD38 by binding to the active site [22]. This binding prevents CD38 from catalyzing the synthesis of cADPR and leads to accumulation of intracellular NAD (+) in dendritic cells, HL-60 cells, and chronic lymphocytic leukemia [23–25]. Therefore, we postulated that C3G might be used to treat RA by inhibiting CD38 activity.…”

Section: Introductionmentioning

confidence: 97%

Potential therapeutic effects of cyanidin-3-O-glucoside on rheumatoid arthritis by relieving inhibition of CD38+ NK cells on Treg cell differentiation

Wang

Zhang

et al. 2019

Arthritis Res Ther

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BackgroundCD38+ NK cells are overabundant in rheumatoid arthritis (RA). Cyanidin-3-O-glucoside (C3G) is an inhibitor of CD38. This study investigated the pathogenic role of CD38+ NK cells and the effect of C3G on RA.MethodsRats with bovine type II collagen-induced arthritis (CIA) were injected with C3G. RA synovial fibroblasts (RASFs) or mononuclear cells (MNCs) were cultured with C3G. MNCs were also cocultured with CD38+ NK cells following C3G pretreatment.ResultsC3G injection significantly alleviated CIA. C3G also significantly increased the level of interleukin (IL)-10 and the regulatory T (Treg) cell proportion, and it decreased the interleukin (IL)-6 and interferon (IFN)-γ levels and CD38+ NK cell proportion in rat peripheral blood and synovial fluid. Additionally, C3G significantly increased RASF apoptosis and decreased RASF proliferation and IL-6 production in the culture medium. Furthermore, C3G stimulated MNCs to increase IL-2 and IL-10 production and the Treg cell proportion, and it caused MNCs to decrease IL-6 and IFN-γ production and the CD38+ NK cell proportion. Although CD38+ NK cells significantly decreased the Treg cell proportion and IL-10 level in MNCs, CD38+ NK cells that had been pretreated with C3G increased the proportion of Treg cells and IL-10 levels and decreased the IL-6 and IFN-γ levels in the coculture. In CD38+ NK cells, C3G significantly increased Sirtuin 6 (Sirt6) expression and the tumor necrosis factor (TNF)-α level, and it decreased natural killer group 2D (NKG2D) expression and the IFN-γ level. However, when CD38+ NK cells were treated with Sirt6 siRNA, C3G did not change the NKG2D expression, the TNF-α level sharply decreased, and the IFN-γ level increased. When MNCs were cocultured with C3G-pretreated CD38+ NK cells in the presence of TNF-α and an anti-IFN-γ antibody, the IL-10+ Treg cell proportion significantly increased. When MNCs were cocultured with C3G-pretreated CD38+ NK cells in the presence of IFN-γ and an anti-TNF-α antibody, the IL-10+ Treg cell proportion sharply decreased. When CIA rats were injected with both C3G and the Sirt6 inhibitor OSS_128167, the rats exhibited joint inflammation and a low Treg cell proportion, but the CD38+ NK proportion was still low.ConclusionC3G has therapeutic effects on CIA and RA. C3G decreased the proportion of CD38+ cells, RASF proliferation, and proinflammatory cytokine secretion, and it increased the Treg cell proportion. C3G also elevated Sirt6 expression to suppress NKG2D expression, increase TNF-α secretion, and decrease IFN-γ secretion in CD38+ NK cells, which stimulates MNCs to differentiate into Treg cells. This study also demonstrates that the inhibition of Treg cell differentiation in MNCs by CD38+ NK cells is a potential cause of the immune imbalance in RA and CIA.

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“…The intensity of the product color, measured at 570 nm, was proportional to the NAD + /NADH concentration in the sample. 22 2.6. Preparation of the Whole-Cell Biocatalyst.…”

Section: Methodsmentioning

confidence: 99%

“…The NAD(H) content in vivo was determined with an NADH/NAD + assay kit (Solarbio Science & Technology Co., Ltd., Beijing, China) following the manufacturer’s protocols. The intensity of the product color, measured at 570 nm, was proportional to the NAD + /NADH concentration in the sample …”

Section: Methodsmentioning

confidence: 99%

Reconstruction of a Cofactor Self-Sufficient Whole-Cell Biocatalyst System for Efficient Biosynthesis of Allitol from d-Glucose

Zhao

Guo

et al. 2022

J. Agric. Food Chem.

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The combined catalysis of glucose isomerase (GI), d-psicose 3-epimerase (DPEase), ribitol dehydrogenase (RDH), and formate dehydrogenase (FDH) provides a convenient route for the biosynthesis of allitol from d-glucose; however, the low catalytic efficiency restricts its industrial applications. Here, the supplementation of 0.32 g/L NAD+ significantly promoted the cell catalytic activity by 1.18-fold, suggesting that the insufficient intracellular NAD(H) content was a limiting factor in allitol production. Glucose dehydrogenase (GDH) with 18.13-fold higher activity than FDH was used for reconstructing a cofactor self-sufficient system, which was combined with the overexpression of the rate-limiting genes involved in NAD+ salvage metabolic flow to expand the available intracellular NAD(H) pool. Then, the multienzyme self-assembly system with SpyTag and SpyCatcher effectively channeled intermediates, leading to an 81.1% increase in allitol titer to 15.03 g/L from 25 g/L d-glucose. This study provided a facilitated strategy for large-scale and efficient biosynthesis of allitol from a low-cost substrate.

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Large changes in NAD levels associated with CD38 expression during HL-60 cell differentiation

Cited by 9 publications

References 29 publications

Intracellular NAD+ levels are associated with LPS-induced TNF-α release in pro-inflammatory macrophages

Intracellular NAD+ levels are associated with LPS-induced TNF-α release in pro-inflammatory macrophages

Potential therapeutic effects of cyanidin-3-O-glucoside on rheumatoid arthritis by relieving inhibition of CD38+ NK cells on Treg cell differentiation

Reconstruction of a Cofactor Self-Sufficient Whole-Cell Biocatalyst System for Efficient Biosynthesis of Allitol from d-Glucose

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