ArticleFrontiers in immunology2021
Titanium Nanoparticles Enhance Production and Suppress Stabilin-1-Mediated Clearance of GDF-15 in Human Primary Macrophages.
Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- Plasma GDF-15 Levels Are Associated With HIV Reservoir Markers Independently of Inflammation in People With HIV on Antiretroviral Therapy.The Journal of infectious diseases · 2026Article
- Zn-doped CaP coating equips Ti implants with corrosion resistance, biomineralization, antibacterial and immunotolerant activities.Journal of advanced research · 2025Article
- Unique transcriptomic responses of rat and human alveolar macrophages in an in vitro model of overload with TiOParticle and fibre toxicology · 2025Article
- Repeated Mesenchymal Stem Cell Delivery Attenuates UHMWPE Wear Particle-Induced Osteolysis by Paracrine-Mediated Macrophage Reprogramming.Journal of inflammation research · 2025Article
- Macrophages as a Source and Target of GDF-15.International journal of molecular sciences · 2024Review
- In vivo assessment of TiOAnalytical and bioanalytical chemistry · 2024Article
- Article
- Modelling of macrophage responses to biomaterialsFrontiers in immunology · 2024Review
- Interaction of Ceramic Implant Materials with Immune System.International journal of molecular sciences · 2023Review
- Tumor-associated macrophages respond to chemotherapy by detrimental transcriptional reprogramming and suppressing stabilin-1 mediated clearance of EGF.Frontiers in immunology · 2023Article
- Immunopathological Inflammation in the Evolution of Mucositis and Peri-Implantitis.International journal of molecular sciences · 2022Article
- Osteoimmune regulation underlies oral implant osseointegration and its perturbation.Frontiers in immunology · 2022Review
- Macrophage scavenger receptors: Tumor support and tumor inhibition.Frontiers in oncology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophages are key innate immune cells that mediate implant acceptance or rejection. Titanium implants degrade over time inside the body, which results in the release of implant wear-off particles. Titanium nanoparticles (TiNPs) favor pro-inflammatory macrophage polarization (M1) and lower tolerogenic activation (M2). GDF-15 regulates immune tolerance and fibrosis and is endocytosed by stabilin-1. How TiNPs affect the healing activities of macrophages and their release of circulating cytokines is an open question in regenerative medicine. In this study for the first time, we identified the transcriptional program induced and suppressed by TiNPs in human pro-inflammatory and healing macrophages. Microarray analysis revealed that TiNPs altered the expression of 5098 genes in M1 (IFN-γ-stimulated) and 4380 genes in M2 (IL-4-stimulated) macrophages. 1980 genes were differentially regulated in both M1 and M2. Affymetrix analysis, confirmed by RT-PCR, demonstrated that TiNPs upregulate expression of GDF-15 and suppress stabilin-1, scavenger receptor of GDF-15. TiNPs also significantly stimulated GDF-15 protein secretion in inflammatory and healing macrophages. Flow cytometry demonstrated, that scavenging activity of stabilin-1 was significantly suppressed by TiNPs. Confocal microscopy analysis showed that TiNPs impair internalization of stabilin-1 ligand acLDL and its transport to the endocytic pathway. Our data demonstrate that TiNPs have a dual effect on the GDF-15/stabilin-1 interaction in macrophage system, by increasing the production of GDF-15 and suppressing stabilin-1-mediated clearance function. In summary, this process can result in a significant increase of GDF-15 in the extracellular space and in circulation leading to unbalanced pro-fibrotic reactions and implant complications.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.