Involvement of thioredoxin reductase 1 in the regulation of redox balance and viability of rheumatoid synovial cells

Kabuyama, Yukihito; Kitamura, Toshio; Yamaki, Junko; Homma, Miwako K.; Kikuchi, Shinichi; Homma, Yoshimi

doi:10.1016/j.bbrc.2007.12.178

Cited by 40 publications

(22 citation statements)

References 24 publications

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“…In particular, TrxR1 is the only enzyme thought to reduce Trx1 in mammalian cells. The late reports also indicated TrxR1 might contribute to the regulation of redox balance and viability of rheumatoid synovial cells [31] , which modulated cellular responses to different cytotoxic agents [32,33] , and provided protection of injured neurons against oxidative stress [34] . The current study demonstrated that TrxR1 mRNA was also simultaneously up-regulated along with Trx1 mRNA in AECⅡ exposed to hyperoxia.…”

Section: Discussionmentioning

confidence: 98%

Effects of hyperoxia on cytoplasmic thioredoxin system in alveolar type epithelial cells of premature rats

Shan

Chang

et al. 2011

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

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This study investigated the effects of hyperoxia on dynamic changes of thioredoxin-1 (Trx1) and thioredoxin reductase-1 (TrxR1) in alveolar type II epithelial cells (AECII) of premature rats. Pregnant Sprague-Dawley rats were sacrificed on day 19 of gestation. AECII were isolated and purified from the lungs of premature rats. When cultured to 80% confluence, in vitro cells were randomly divided into air group and hyperoxia group. Cells in the hyperoxia group were continuously exposed to 95% O(2)/5% CO(2) and those in the air group to 95% air/5% CO(2). After 12, 24 and 48 h, cells in the two groups were harvested to detect their reactive oxygen species (ROS), apoptosis, TrxR1 activity and the expressions of Trx1 and TrxR1 by corresponding protocols, respectively. The results showed that AEC II exposed to hyperoxia generated excessive ROS and the apoptosis percentage in the hyperoxia group was increased significantly at each time points as compared with that in the air group (P<0.001). Moreover, TrxR1 activity was found to be markedly depressed in the hyperoxia group in comparison to that in the air group (P<0.001). RT-PCR showed the expressions of both Trx1 and TrxR1 mRNA were significantly increased in AECII exposed to hyperoxia for 12 and 24 h (P<0.01), respectively. At 48 h, the level of Trx1 mRNA as well as that of TrxR1 mRNA in the hyperoxia group was reduced and showed no significant difference from that in the air group (P>0.05). Western blotting showed the changes of Trx1 protein expressions in the hyperoxia group paralleled those of Trx1 mRNA expressions revealed by RT-PCR. It was concluded that hyperoxia can up-regulate the protective Trx1/TrxR1 expressed by AECII in a certain period, however, also cause dysfunction of the cytoplasmic thioredoxin system by decreasing TrxR1 activity, which may contribute to the progression of oxidative stress and cell apoptosis and finally result in lung injury.

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Section: Discussionmentioning

confidence: 98%

Effects of hyperoxia on cytoplasmic thioredoxin system in alveolar type epithelial cells of premature rats

Shan

Chang

et al. 2011

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

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“…In addition, TrxR is involved in the redox activity of RAW264.7 macrophages [54][55][56]. Our interest in examining the binding of gold complexes, and possibly Au NPs, to TrxR was derived in part from the contribution that these interactions may make to their anti-arthritic activity [18,19].…”

Section: Thioredoxin Reductase Binding Studiesmentioning

confidence: 99%

“…Both Trx and TrxR are over-expressed in synovial cells or fluid of RA patients [18,19]. Inhibition of TrxR by gold drugs has attracted interest due to the presence of a selenocysteine residue at its active site, and the greater affinity of Au(I) for selenol groups compared to thiols [20,21].…”

Section: Introductionmentioning

confidence: 99%

An investigation into the interactions of gold nanoparticles and anti-arthritic drugs with macrophages, and their reactivity towards thioredoxin reductase

James

Sluyter

et al. 2015

Journal of Inorganic Biochemistry

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“…Consequently, T cell-associated CD28 interacts effectively with antigen-presenting cell co-stimulatory molecule, B7, thereby enhancing survival of memory cells in the absence of T cell receptor activation. Analysis of the transcriptome of rheumatoid synovial cells has revealed the upregulation of thioredoxin reductase 1, the activity of which restores the thioredoxin redox couple (139) and an enzyme which works with the glutaredoxin system to maintain a reduced state for cellular protein thiols. These data suggest that synovial cells are able to adapt and to survive in an oxidizing environment where GSH is lost; the thioredoxin= thioredoxin reductase cycle may be preferentially induced to provide an alternative strategy for restoring oxidized cysteine residues.…”

mentioning

confidence: 99%

Aberrant Reactive Oxygen and Nitrogen Species Generation in Rheumatoid Arthritis (RA): Causes and Consequences for Immune Function, Cell Survival, and Therapeutic Intervention

Phillips

Dias

Kitas

et al. 2010

Antioxidants & Redox Signaling

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The infiltration and persistence of hematopoietic immune cells within the rheumatoid arthritis (RA) joint results in elevated levels of pro-inflammatory cytokines, increased reactive oxygen (ROS) and -nitrogen (RNS) species generation, that feeds a continuous self-perpetuating cycle of inflammation and destruction. Meanwhile, the controlled production of ROS is required for signaling within the normal physiological reaction to perceived "foreign matter" and for effective apoptosis. This review focuses on the signaling pathways responsible for the induction of the normal immune response and the contribution of ROS to this process. Evidence for defects in the ability of immune cells in RA to regulate the generation of ROS and the consequence for their immune function and for RA progression is considered. As the hypercellularity of the rheumatoid joint and the associated persistence of hematopoietic cells within the rheumatoid joint are symptomatic of unresponsiveness to apoptotic stimuli, the role of apoptotic signaling proteins (specifically Bcl-2 family members and the tumor suppressor p53) as regulators of ROS generation and apoptosis are considered, evaluating evidence for their aberrant expression and function in RA. We postulate that ROS generation is required for effective therapeutic intervention.

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Involvement of thioredoxin reductase 1 in the regulation of redox balance and viability of rheumatoid synovial cells

Cited by 40 publications

References 24 publications

Effects of hyperoxia on cytoplasmic thioredoxin system in alveolar type epithelial cells of premature rats

Effects of hyperoxia on cytoplasmic thioredoxin system in alveolar type epithelial cells of premature rats

An investigation into the interactions of gold nanoparticles and anti-arthritic drugs with macrophages, and their reactivity towards thioredoxin reductase

Aberrant Reactive Oxygen and Nitrogen Species Generation in Rheumatoid Arthritis (RA): Causes and Consequences for Immune Function, Cell Survival, and Therapeutic Intervention

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