Inhibition of TNF-α, IL-1α, and IL-1β by Pretreatment of Human Monocyte-Derived Macrophages with Menaquinone-7 and Cell Activation with TLR Agonists <i>In Vitro</i>

Pan, Min‐Hsiung; Maresz, Katarzyna; Lee, Pei Sheng; Wu, Juan; Ho, Chi Tang; Popko, Janusz; Mehta, Dilip; Stohs, Sidney J.; Badmaev, Vladimir

doi:10.1089/jmf.2016.0030

Cited by 49 publications

(38 citation statements)

References 15 publications

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“…MK-4 suppressed LPS-induced expression of inflammatory cytokines such as IL-6 in macrophage-like cells and MG-6 mouse microglia-derived cells through the inhibition of NF-κB signaling pathway [16,45]. Pretreatment with MK-7 inhibited the production of TNF-α after the toll-like receptor (TLR) activation in human monocyte-derived macrophages [17]. LPS-induced production of IL-6 in human fibroblasts is intensively inhibited by naphthoquinone compounds [46].…”

Section: Anti-inflammatory Effects Of Vitamin Kmentioning

confidence: 99%

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The Inhibitory Roles of Vitamin K in Progression of Vascular Calcification

et al. 2020

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Vitamin K is a fat-soluble vitamin that is indispensable for the activation of vitamin K-dependent proteins (VKDPs) and may be implicated in cardiovascular disease (CVD). Vascular calcification is intimately associated with CV events and mortality and is a chronic inflammatory process in which activated macrophages promote osteoblastic differentiation of vascular smooth muscle cells (VSMCs) through the production of proinflammatory cytokines such as IL-1β, IL-6, TNF-α, and oncostatin M (OSM) in both intimal and medial layers of arterial walls. This process may be mainly mediated through NF-κB signaling pathway. Vitamin K has been demonstrated to exert anti-inflammatory effects through antagonizing NF-κB signaling in both in vitro and in vivo studies, suggesting that vitamin K may prevent vascular calcification via anti-inflammatory mechanisms. Matrix Gla protein (MGP) is a major inhibitor of soft tissue calcification and contributes to preventing both intimal and medial vascular calcification. Vitamin K may also inhibit progression of vascular calcification by enhancing the activity of MGP through facilitating its γ-carboxylation. In support of this hypothesis, the procalcific effects of warfarin, an antagonist of vitamin K, on arterial calcification have been demonstrated in several clinical studies. Among the inactive MGP forms, dephospho-uncarboxylated MGP (dp-ucMGP) may be regarded as the most useful biomarker of not only vitamin K deficiency, but also vascular calcification and CVD. There have been several studies showing the association of circulating levels of dp-ucMGP with vitamin K intake, vascular calcification, mortality, and CVD. However, additional larger prospective studies including randomized controlled trials are necessary to confirm the beneficial effects of vitamin K supplementation on CV health.

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Section: Anti-inflammatory Effects Of Vitamin Kmentioning

confidence: 99%

“…Vitamin K status was inversely associated with circulating inflammatory markers such as IL-6 and C-reactive protein (CRP) [14]. Vitamin K attenuated lipopolysaccharide (LPS)-induced inflammatory responses by blocking nuclear factor κB (NF-κB) signal transduction [15][16][17].…”

Section: Introductionmentioning

confidence: 99%

The Inhibitory Roles of Vitamin K in Progression of Vascular Calcification

et al. 2020

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“…For example, eATP released by damaged cells can activate the immune system via the stimulation of P2X7 receptors on DCs and then promote the secretion of IL-1β and IL-18 (31). Next, IL-1β will facilitate macrophages maturation and their cytokine production increase (32). Similarly, IL-18 would boost NK cells proliferation and strengthen IFN-γ production plus cytotoxicity (33).…”

Section: Classic Features Of Cd39mentioning

confidence: 99%

What Else Can CD39 Tell Us?

et al. 2017

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As the rate-limiting enzyme in ATP/ADP–AMP–adenosine pathway, CD39 would be a novel checkpoint inhibitor target in preventing adenosine-triggered immune-suppressive effect. In addition, CD39hi Tregs, but not CD25hi Tregs, exhibit sustained Foxp3 levels and functional abilities, indicating it could represent a new specific marker of Tregs. Similarly, inhibition of CD39 enzymatic function at the surface of tumor cells alleviates their immunosuppressive activity. Far from conclusive, present research revealed that CD39 also dephosphorylated and thus inactivated self- and pathogen-associated phosphoantigens of Vγ9Vδ2 T cells, which may be the most promising subpopulation for cellular vaccine. CD39 is also tightly related to Th17 cells and can be regarded as a Th17 cells marker. In this review, we focus on present research of CD39 ectoenzyme and provide insights into its clinical application.

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“…Nevertheless one study disclosed that menaquinone can suppress the expression of TLR2 and TLR4 as well as inhibit calcification of aortic intima and smooth muscle cells in ApoE −/− mice [ 221 ]. Moreover, in vitro pretreatment of human monocyte-derived macrophages with menaquinone-7 for 30 h and subsequent activation with TLR agonists resulted in inhibition of pro-inflammatory cytokine production [ 222 ]. Abovementioned outcomes allow concluding that vitamin D and K2 have a synergistic effect and dual supplementation may provide an added benefit for patients’ bone and cardiovascular health.…”

Section: Toll-like Receptors and Vitamin Dmentioning

confidence: 99%

The Role of Toll-Like Receptors and Vitamin D in Cardiovascular Diseases—A Review

Adamczak

2017

IJMS

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Cardiovascular diseases are the leading cause of mortality worldwide. Therefore, a better understanding of their pathomechanisms and the subsequent implementation of optimal prophylactic and therapeutic strategies are of utmost importance. A growing body of evidence states that low-grade inflammation is a common feature for most of the cardiovascular diseases in which the contributing factors are the activation of toll-like receptors (TLRs) and vitamin D deficiency. In this article, available data concerning the association of cardiovascular diseases with TLRs and vitamin D status are reviewed, followed by a discussion of new possible approaches to cardiovascular disease management.

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Inhibition of TNF-α, IL-1α, and IL-1β by Pretreatment of Human Monocyte-Derived Macrophages with Menaquinone-7 and Cell Activation with TLR Agonists In Vitro

Cited by 49 publications

References 15 publications

The Inhibitory Roles of Vitamin K in Progression of Vascular Calcification

The Inhibitory Roles of Vitamin K in Progression of Vascular Calcification

What Else Can CD39 Tell Us?

The Role of Toll-Like Receptors and Vitamin D in Cardiovascular Diseases—A Review

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