Taurine chloramine inhibits proliferation of rheumatoid arthritis synoviocytes by triggering a p53-dependent pathway

Kontny, Ewa; Rudnicka, W; Chorąży-Massalska, Magdalena; Marcinkiewicz, Janusz; Maśliński, Włodzimierz

doi:10.1007/s00011-006-5067-5

Cited by 22 publications

(10 citation statements)

References 54 publications

(80 reference statements)

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“…Kontny et al . reported that TauCl caused progressive necrosis of RA FLS at ≥500 µM [36]. However, in our previous report, TauCl toxicity seemed to vary according to the individual RA patient [16].…”

Section: Discussionmentioning

confidence: 92%

Effect of taurine chloramine on the production of matrix metalloproteinases (MMPs) in adiponectin- or IL-1β-stimulated fibroblast-like synoviocytes

Kim

Choi

et al. 2010

J Biomed Sci

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BackgroundAdiponectin greatly stimulated the expression of matrix metalloproteinases (MMPs) in fibroblast-like synoviocytes (FLSs) as did IL-1β. We wondered whether taurine chloramine (TauCl) inhibits the production of MMPs stimulated by adiponectin in the same pattern as by IL-1β stimulation in vitroMethodsSynovial cells from rheumatoid arthritis (RA) patients were treated with adiponectin or interleukin (IL)-1β for 24 hr in the presence or absence of TauCl. The culture supernatant was collected and the levels of MMPs were measured by enzyme-linked immunosorbent assay (ELISA). The IκB signaling pathways stimulated by adiponectin were studied and the levels of NF-κB in the nuclei of the cells were analyzed by ELISA.ResultsTauCl (600 µM) inhibited MMP-13, but not MMP-1, expression in IL-1β-stimulated RA FLSs. However, TauCl at the same concentration significantly inhibited the production of both adiponectin-stimulated MMP-1 and MMP-13 expression. TauCl inhibited the degradation of IκB-α stimulated by adiponectin, but not by IL-1β. Similarly, the level of NF-κB in the nucleus was increased by adiponectin stimulation and was inhibited by 600 µM TauCl. However, the levels of NF-κB increased by IL-1β stimulation were not inhibited by 600 µM TauCl.ConclusionsTauCl more effectively inhibited MMPs expression induced by adiponectin than that by IL-1β in RA FLS, suggesting that TauCl plays an important role in down-regulating the expression of MMPs in arthritic joints.

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Section: Discussionmentioning

confidence: 92%

Effect of taurine chloramine on the production of matrix metalloproteinases (MMPs) in adiponectin- or IL-1β-stimulated fibroblast-like synoviocytes

Kim

Choi

et al. 2010

J Biomed Sci

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“…Moreover, in these cells TauCl down-regulates also expression of collagenases (MMP-1, MMP-13) that play a dominant destructive role in RA (Kim et al 2007, 2010a, b). Furthermore, TauCl inhibits proliferation of RA FLS and renders these cells more sensitive to death (Kontny et al 2006a, b). Thus, in vitro TauCl dampens several activities of rheumatoid FLS relevant to the contribution of these cells to local pathological processes, i.e., inflammation support, joint destruction and synovial hyperplasia.…”

Section: Taurine and Taurine Derivatives In Rheumatoid Arthritis (Ra)mentioning

confidence: 99%

Taurine and inflammatory diseases

Marcinkiewicz

Kontny²

2012

Amino Acids

421

333

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Taurine (2-aminoethanesulfonic acid) is the most abundant free amino acid in humans and plays an important role in several essential biological processes such as bile acid conjugation, maintenance of calcium homeostasis, osmoregulation and membrane stabilization. Moreover, attenuation of apoptosis and its antioxidant activity seem to be crucial for the cytoprotective effects of taurine. Although these properties are not tissue specific, taurine reaches particularly high concentrations in tissues exposed to elevated levels of oxidants (e.g., inflammatory cells). It suggests that taurine may play an important role in inflammation associated with oxidative stress. Indeed, at the site of inflammation, taurine is known to react with and detoxify hypochlorous acid generated by the neutrophil myeloperoxidase (MPO)–halide system. This reaction results in the formation of less toxic taurine chloramine (TauCl). Both haloamines, TauCl and taurine bromamine (TauBr), the product of taurine reaction with hypobromous acid (HOBr), exert antimicrobial and anti-inflammatory properties. In contrast to a well-documented regulatory role of taurine and taurine haloamines (TauCl, TauBr) in acute inflammation, their role in the pathogenesis of inflammatory diseases is not clear. This review summarizes our current knowledge concerning the role of taurine, TauCl and TauBr in the pathogenesis of inflammatory diseases initiated or propagated by MPO-derived oxidants. The aim of this paper is to show links between inflammation, neutrophils, MPO, oxidative stress and taurine. We will discuss the possible contribution of taurine and taurine haloamines to the pathogenesis of inflammatory diseases, especially in the best studied example of rheumatoid arthritis.

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“…It has been suggested and demonstrated for many systems that N-chloroamino acids, formed upon reaction with HOCl/OCl ( , decrease the concentration of this chlorinating agent but exert similar effects themselves. Taurine has been reported to prevent the production of nitrite and TNF-a by lung cells in the presence of myeloperoxidase-H 2 O 2 -halide system via N-chlorotaurine formation [30], but on the other hand N-chlorotaurine has also been implicated in intracellular glutathione loss [31] and apoptosis induction by triggering the p-53 dependent pathway [32]. Amine group of proteins, apart from thiols, are the major targets of HOCl/OCl ( acid attack in proteins [8].…”

Section: Discussionmentioning

confidence: 99%

Effect of N-chloroamino acids on the erythrocyte

Robaszkiewicz

Bartosz

Soszyński

2008

Free Radical Research

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Amino acids present in blood plasma may be targets for oxidation and chlorination by HOCl/OCl(-). N-Chloroamino acids have been reported to be less reactive, but more selective than HOCl/OCl(-) in their reactions; therefore, they may act as secondary mediators of HOCl/OCl(-)-induced injury. This study compared the effects of five N-chloroamino acids (AlaCl, LysCl, SerCl, AspCl and PheCl) on erythrocytes with the action of HOCl/OCl(-). The N-chloroamino acids differed in stability and reactivity. They had a weaker haemolytic action than HOCl/OCl(-); HOCl/OCl(-), AlaCl and PheCl increased osmotic fragility of erythrocytes at a concentration of 1 mm. Oxidation of glutathione, formation of protein-glutathione mixed disulphides and efflux of GSSG from erythrocytes were observed for erythrocytes treated with all the employed chloroderivatives, while increased oxidation of 2',7'-dichlorofluorescin was detected only after treatment of the cells with 1 mm HOCl/OCl(-), AlaCl and PheCl. Generally, the reactivity of at least some N-chloroamino acids may be not much lower with respect to HOCl/OCl(-).

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Taurine chloramine inhibits proliferation of rheumatoid arthritis synoviocytes by triggering a p53-dependent pathway

Abstract: We propose that Tau-Cl inhibits proliferation of RA FLS by triggering a p53-dependent cell-cycle arrest and conclude that this compound suppresses pathways in FLS that are known to contribute to the pathology of RA.

Cited by 22 publications

References 54 publications

Effect of taurine chloramine on the production of matrix metalloproteinases (MMPs) in adiponectin- or IL-1β-stimulated fibroblast-like synoviocytes

Effect of taurine chloramine on the production of matrix metalloproteinases (MMPs) in adiponectin- or IL-1β-stimulated fibroblast-like synoviocytes

Taurine and inflammatory diseases

Effect of N-chloroamino acids on the erythrocyte

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