The influence of Ni(II) on surface antigen expression in murine macrophages

D’Antò, Vincenzo; Eckhardt, Alexander; Hiller, Karl Anton; Spagnuolo, Gianrico; Valletta, Rosa; Ambrosio, Luigi; Schmalz, Gottfried; Schweikl, Helmut

doi:10.1016/j.biomaterials.2008.12.004

Cited by 36 publications

(29 citation statements)

References 52 publications

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“…1D, right panel) were identified by CD11b and F4/80 expression (data not shown). Macrophage activation markers (CD14, CD40, CD80, and CD86) (Tacke and Randolph 2006;D'Anto et al 2009) were increased in LPS-treated CD11b and F4/80 positive cells (Fig. 1D).…”

Section: Identification Of Hnrnp K-associated Mrnas Affected In Macromentioning

confidence: 88%

Translation control of TAK1 mRNA by hnRNP K modulates LPS-induced macrophage activation

Liepelt

Mossanen

Denecke

et al. 2014

RNA

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Macrophage activation by bacterial lipopolysaccharides (LPS) is induced through Toll-like receptor 4 (TLR4). The synthesis and activity of TLR4 downstream signaling molecules modulates the expression of pro-and anti-inflammatory cytokines. To address the impact of post-transcriptional regulation on that process, we performed RIP-Chip analysis. Differential association of mRNAs with heterogeneous nuclear ribonucleoprotein K (hnRNP K), an mRNA-specific translational regulator in differentiating hematopoietic cells, was studied in noninduced and LPS-activated macrophages. Analysis of interactions affected by LPS revealed several mRNAs encoding TLR4 downstream kinases and their modulators. We focused on transforming growth factor-β-activated kinase 1 (TAK1) a central player in TLR4 signaling. HnRNP K interacts specifically with a sequence in the TAK1 mRNA 3 ′ UTR in vitro. Silencing of hnRNP K does not affect TAK1 mRNA synthesis or stability but enhances TAK1 mRNA translation, resulting in elevated TNF-α, IL-1β, and IL-10 mRNA expression. Our data suggest that the hnRNP K-3 ′ UTR complex inhibits TAK1 mRNA translation in noninduced macrophages. LPS-dependent TLR4 activation abrogates translational repression and newly synthesized TAK1 boosts macrophage inflammatory response.

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Section: Identification Of Hnrnp K-associated Mrnas Affected In Macromentioning

confidence: 88%

Translation control of TAK1 mRNA by hnRNP K modulates LPS-induced macrophage activation

Liepelt

Mossanen

Denecke

et al. 2014

RNA

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“…Ni ions are considered the principal cytotoxic agents released by orthodontic alloys 16 ; higher concentrations of this element likely cause toxic effects and might play a role in the innate immune response to metal biomaterials. 17 Nevertheless, the time-dependent cytotoxicity observed for Sentalloy High Aesthetic, BioCosmetic, and EverWhite might depend on two distinct factors: an increasing concentration of metallic ions in the medium over time or a continuous release of substances as a result of the biodegradation of the esthetic coating.…”

Section: Discussionmentioning

confidence: 99%

In vitro biocompatibility of nickel-titanium esthetic orthodontic archwires

Rongo

Valletta

Bucci

et al. 2016

The Angle Orthodontist

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Objective: To investigate the cytotoxicity of nickel-titanium (NiTi) esthetic orthodontic archwires with different surface coatings. Materials and Methods: Three fully coated, tooth-colored NiTi wires (BioCosmetic, Titanol Cosmetic, EverWhite), two ion-implanted wires (TMA Purple, Sentalloy High Aesthetic), five uncoated NiTi wires (BioStarter, BioTorque, Titanol Superelastic, Memory Wire Superelastic, and Sentalloy), one b-titanium wire (TMA), and one stainless steel wire (Stainless Steel) were considered for this study. The wire samples were placed at 37uC in airtight test tubes containing Dulbecco's Modified Eagle's Medium (0.1 mg/mL) for 1, 7, 14, and 30 days. The cell viability of human gingival fibroblasts (HGFs) cultured with this medium was assessed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Data were analyzed by a twoway analysis of variance (a 5 .05). Results: The highest cytotoxic effect was reached on day 30 for all samples. The archwires exhibited a cytotoxicity on HGFs ranging from "none" to "slight," with the exception of the BioTorque, which resulted in moderate cytotoxicity on day 30. Significant differences were found between esthetic archwires and their uncoated pairs only for BioCosmetic (P 5 .001) and EverWhite (P , .001). Conclusions: Under the experimental conditions, all of the NiTi esthetic archwires resulted in slight cytotoxicity, as did the respective uncoated wires. For this reason their clinical use may be considered to have similar risks to the uncoated archwires. (Angle Orthod. 2016;86:789-795.)

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“…Flow cytometry acquisition was performed on FACScan ® flow cytometer and data were analyzed using CellQuest TM software (BD Biosciences). The percentage of cells positive for each surface protein was determined based upon isotype control staining, and the amount of surface antigen expression of all cells counted was calculated by the following equation: Expression Index (EI)=% positive cells×Mean Fluorescence Intensity [25] .…”

Section: Macrophage Surface Antigen Expressionmentioning

confidence: 99%

Immunomodulatory activity of andrographolide on macrophage activation and specific antibody response

et al. 2010

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Aim: To investigate the immunomodulatory effects of andrographolide on both innate and adaptive immune responses. Methods: Andrographolide (10 µg/mL in vitro or 1 mg/kg in vivo) was used to modulate LPS-induced classical activated (M1) or IL-4-induced alternative activated (M2) macrophages in vitro and humor immune response to HBsAg in vivo. Cytokine gene expression profile (M1 vs M2) was measured by real-time PCR, IL-12/IL-10 level was detected by ELISA, and surface antigen expression was evaluated by flow cytometry, whereas phosphorylation level of ERK 1/2 and AKT was determined by Western blot. The level of anti-HBs antibodies in HBsAg immunized mice was detected by ELISA, and the number of HBsAg specific IL-4-producing splenocyte was enumerated by ELISPOT. Results: Andrographolide treatment in vitro attenuated either LPS or IL-4 induced macrophage activation, inhibited both M1 and M2 cytokines expression and decreased IL-12/IL-10 ratio (the ratio of M1/M2 polarization). Andrographolide down-regulated the expression of mannose receptor (CD206) in IL-4 induced macrophages and major histocompability complex/costimulatory molecules (MHC I, CD40, CD80, CD86) in LPS-induced macrophages. Correspondingly, anti-HBs antibody production and the number of IL-4-producing splenocytes were reduced by in vivo administration of andrographolide. Reduced phosphorylation levels of ERK1/2 and AKT were observed in macrophages treated with andrographolide. Conclusion: Andrographolide can modulate the innate and adaptive immune responses by regulating macrophage phenotypic polarization and Ag-specific antibody production. MAPK and PI3K signaling pathways may participate in the mechanisms of andrographolide regulating macrophage activation and polarization.

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The influence of Ni(II) on surface antigen expression in murine macrophages

Cited by 36 publications

References 52 publications

Translation control of TAK1 mRNA by hnRNP K modulates LPS-induced macrophage activation

Translation control of TAK1 mRNA by hnRNP K modulates LPS-induced macrophage activation

In vitro biocompatibility of nickel-titanium esthetic orthodontic archwires

Immunomodulatory activity of andrographolide on macrophage activation and specific antibody response

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