ArticleScientific reports2021
Proteomic and genomic analysis of acid dentin lysate with focus on TGF-β signaling.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed, 11 citations in OpenAlex.
- Bone Allograft Acid Lysates Change the Genetic Signature of Gingival Fibroblasts.International journal of molecular sciences · 2023Article
- Gingival Fibroblasts Are Sensitive to Oral Cell Lysates Indicated by Their IL11 Expression.Bioengineering (Basel, Switzerland) · 2023Article
- Article
- Acid Dentin Lysate Modulates Macrophage Polarization and Osteoclastogenesis In Vitro.Materials (Basel, Switzerland) · 2021Article
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Authors and funding
7 authors at 4 institutions in 4 countries.
Funding
Abstract
Particulate autologous tooth roots are increasingly used for alveolar bone augmentation; however, the proteomic profile of acid dentin lysate and the respective cellular response have not been investigated. Here we show that TGF-β1 is among the 226 proteins of acid dentin lysate (ADL) prepared from porcine teeth. RNA sequencing identified 231 strongly regulated genes when gingival fibroblasts were exposed to ADL. Out of these genes, about one third required activation of the TGF-β receptor type I kinase including interleukin 11 (IL11) and NADPH oxidase 4 (NOX4). Reverse transcription-quantitative polymerase chain reaction and immunoassay confirmed the TGF-β-dependent expression of IL11 and NOX4. The activation of canonical TGF-β signaling by ADL was further confirmed by the phosphorylation of Smad3 and translocation of Smad2/3, using Western blot and immunofluorescence staining, respectively. Finally, we showed that TGF-β activity released from dentin by acid lysis adsorbs to titanium and collagen membranes. These findings suggest that dentin particles are a rich source of TGF-β causing a major response of gingival fibroblasts.
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Registered trials
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