Inflammatory degeneration of joint tissue in adjuvant arthritis after intraarticular treatment with the mixture of silver drug and nicotinic acid

Mitrofanov, V. A.; Ovchinnikova, N M; Белова, С В; Федотова, М. В.; Гладкова, Е. В.

doi:10.1007/s10517-006-0059-6

Cited by 4 publications

(3 citation statements)

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“…In addition, HCA2 has been found to be expressed by various immune cells including macrophages, neutrophils, and epidermal Langerhans cells 19 20 41 42 , and the expression in macrophages is increased by treatment with IFN-γ in combination with TNF-α, lipopolysaccharide, and CpG oligodeoxynucleotides 20 . Recent studies revealed that niacin possesses anti-inflammatory activities in various tissues/cell types via HCA2 18 27 28 29 30 43 44 . Interestingly, activation of HCA2 by niacin significantly inhibited chemokine-induced migration of macrophages 18 34 .…”

Section: Discussionmentioning

confidence: 99%

“…Niacin has been shown to suppress TNF-α-induced release of proinflammatory chemokines thus reducing chemokine MCP-1 (CCL2)-induced recruitment of macrophages into the atherosclerotic lesions 18 24 25 26 . Interestingly, recent in vitro and in vivo studies have revealed anti-inflammatory roles of niacin in acute ischemic stroke, arthritis, chronic renal failure and sepsis 27 28 29 30 31 32 , suggesting that niacin not only inhibits vascular inflammation, but also has therapeutic potential in other systemic inflammatory and metabolic diseases.…”

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confidence: 99%

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Activated niacin receptor HCA2 inhibits chemoattractant-mediated macrophage migration via Gβγ/PKC/ERK1/2 pathway and heterologous receptor desensitization

Shi

Lai

et al. 2017

Sci Rep

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The niacin receptor HCA2 is implicated in controlling inflammatory host responses with yet poorly understood mechanistic basis. We previously reported that HCA2 in A431 epithelial cells transduced Gβγ-protein kinase C- and Gβγ-metalloproteinase/EGFR-dependent MAPK/ERK signaling cascades. Here, we investigated the role of HCA2 in macrophage-mediated inflammation and the underlying mechanisms. We found that proinflammatory stimulants LPS, IL-6 and IL-1β up-regulated the expression of HCA2 on macrophages. Niacin significantly inhibited macrophage chemotaxis in response to chemoattractants fMLF and CCL2 by disrupting polarized distribution of F-actin and Gβ protein. Niacin showed a selected additive effect on chemoattractant-induced activation of ERK1/2, JNK and PI3K pathways, but only the MEK inhibitor UO126 reduced niacin-mediated inhibition of macrophage chemotaxis, while activation of ERK1/2 by EGF alone did not inhibit fMLF-mediated migration of HEK293T cells co-expressing HCA2 and fMLF receptor FPR1. In addition, niacin induced heterologous desensitization and internalization of FPR1. Furthermore, niacin rescued mice from septic shock by diminishing inflammatory symptoms and the effect was abrogated in HCA2−/− mice. These results suggest that Gβγ/PKC-dependent ERK1/2 activation and heterologous desensitization of chemoattractant receptors are involved in the inhibition of chemoattractant-induced migration of macrophages by niacin. Thus, HCA2 plays a critical role in host protection against pro-inflammatory insults.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Activated niacin receptor HCA2 inhibits chemoattractant-mediated macrophage migration via Gβγ/PKC/ERK1/2 pathway and heterologous receptor desensitization

Shi

Lai

et al. 2017

Sci Rep

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“…A niacinmediated beneficial cardiovascular effect has been shown to be transferable with GPR109A-competent bone marrow cells (21). In addition, accumulating evidence has demonstrated that activation of GPR109A was able to induce anti-inflammatory effects not only on atherosclerosis but also on acute ischemic stroke, arthritis, chronic renal failure, and sepsis through inhibition of immune cell chemotaxis and proinflammatory cytokine production (20)(21)(22)(23)(24)(25)(26)(27)(28)(29). Therefore, more studies are needed to thoroughly evaluate the GPR109A-mediated pleiotropic effects on atherogenesis and other metabolic diseases.…”

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confidence: 99%

Niacin fine‐tunes energy homeostasis through canonical GPR109A signaling

Cao

Lai

et al. 2018

FASEB j.

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The incidence of overweight and obesity has become a global public health problem, constituting a major risk factor for numerous comorbidities. Despite tremendous efforts, effective pharmacological agents for the treatment of obesity are still limited. Here, we showed that in contrast to lactate receptor GPR81, niacin receptor GPR109A‐deficient mice had progressive weight gain and hepatic fat accumulation. Using high‐fat diet–induced mouse model of obesity, we demonstrated that niacin treatment apparently protected against obesity without affecting food intake in wild‐type mice but not in GPR109A‐deficient mice. Further investigation showed that niacin treatment led to a remarkable inhibition of hepatic de novo lipogenesis. Additionally, we demonstrated that niacin treatment triggered brown adipose tissue and/or white adipose tissue thermogenic activity via activation of GPR109A. Moreover, we observed that mice exposed to niacin exhibited a dramatic decrease in intestinal absorption of sterols and fatty acids. Taken together, our findings demonstrate that acting on GPR109A, niacin shows the potential to maintain energy homeostasis through multipathways, representing a potential approach to the treatment of obesity, diabetes and cardiovascular disease.—Ye, L., Cao, Z., Lai, X., Wang, W., Guo, Z., Yan, L., Wang, Y., Shi, Y., Zhou, N. Niacin fine‐tunes energy homeostasis through canonical GPR109A signaling. FASEB J. 33, 4765–4779 (2019). http://www.fasebj.org

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Nicotinic acid (niacin): new lipid-independent mechanisms of action and therapeutic potentials

Lukasova

Hanson

Tunaru

et al. 2011

Trends in Pharmacological Sciences

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Inflammatory degeneration of joint tissue in adjuvant arthritis after intraarticular treatment with the mixture of silver drug and nicotinic acid

Cited by 4 publications

References 1 publication

Activated niacin receptor HCA2 inhibits chemoattractant-mediated macrophage migration via Gβγ/PKC/ERK1/2 pathway and heterologous receptor desensitization

Activated niacin receptor HCA2 inhibits chemoattractant-mediated macrophage migration via Gβγ/PKC/ERK1/2 pathway and heterologous receptor desensitization

Niacin fine‐tunes energy homeostasis through canonical GPR109A signaling

Nicotinic acid (niacin): new lipid-independent mechanisms of action and therapeutic potentials

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