SiONx Coating Regulates Mesenchymal Stem Cell Antioxidant Capacity via Nuclear Erythroid Factor 2 Activity under Toxic Oxidative Stress Conditions

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dc.citation.articleNumber189en_US
dc.citation.issueNumber2en_US
dc.citation.journalTitleAntioxidantsen_US
dc.citation.volumeNumber13en_US
dc.contributor.authorAhuja, Neelamen_US
dc.contributor.authorAwad, Kamalen_US
dc.contributor.authorYang, Suen_US
dc.contributor.authorDong, Heen_US
dc.contributor.authorMikos, Antoniosen_US
dc.contributor.authorAswath, Praneshen_US
dc.contributor.authorYoung, Simonen_US
dc.contributor.authorBrotto, Marcoen_US
dc.contributor.authorVaranasi, Venuen_US
dc.contributor.orgCenter for Engineering Complex Tissuesen_US
dc.contributor.orgCenter for Excellence in Tissue Engineeringen_US
dc.date.accessioned2024-07-25T20:56:27Zen_US
dc.date.available2024-07-25T20:56:27Zen_US
dc.date.issued2024en_US
dc.description.abstractHealing in compromised and complicated bone defects is often prolonged and delayed due to the lack of bioactivity of the fixation device, secondary infections, and associated oxidative stress. Here, we propose amorphous silicon oxynitride (SiONx) as a coating for the fixation devices to improve both bioactivity and bacteriostatic activity and reduce oxidative stress. We aimed to study the effect of increasing the N/O ratio in the SiONx to fine-tune the cellular activity and the antioxidant effect via the NRF2 pathway under oxidative stress conditions. The in vitro studies involved using human mesenchymal stem cells (MSCs) to examine the effect of SiONx coatings on osteogenesis with and without toxic oxidative stress. Additionally, bacterial growth on SiONx surfaces was studied using methicillin-resistant Staphylococcus aureus (MRSA) colonies. NRF2 siRNA transfection was performed on the hMSCs (NRF2-KD) to study the antioxidant response to silicon ions. The SiONx implant surfaces showed a >4-fold decrease in bacterial growth vs. bare titanium as a control. Increasing the N/O ratio in the SiONx implants increased the alkaline phosphatase activity >1.5 times, and the other osteogenic markers (osteocalcin, RUNX2, and Osterix) were increased >2-fold under normal conditions. Increasing the N/O ratio in SiONx enhanced the protective effects and improved cell viability against toxic oxidative stress conditions. There was a significant increase in osteocalcin activity compared to the uncoated group, along with increased antioxidant activity under oxidative stress conditions. In NRF2-KD cells, there was a stunted effect on the upregulation of antioxidant markers by silicon ions, indicating a role for NRF2. In conclusion, the SiONx coatings studied here displayed bacteriostatic properties. These materials promoted osteogenic markers under toxic oxidative stress conditions while also enhancing antioxidant NRF2 activity. These results indicate the potential of SiONx coatings to induce in vivo bone regeneration in a challenging oxidative stress environment.en_US
dc.identifier.citationAhuja, N., Awad, K., Yang, S., Dong, H., Mikos, A., Aswath, P., Young, S., Brotto, M., & Varanasi, V. (2024). SiONx Coating Regulates Mesenchymal Stem Cell Antioxidant Capacity via Nuclear Erythroid Factor 2 Activity under Toxic Oxidative Stress Conditions. Antioxidants, 13(2), Article 2. https://doi.org/10.3390/antiox13020189en_US
dc.identifier.digitalantioxidants-13-00189en_US
dc.identifier.doihttps://doi.org/10.3390/antiox13020189en_US
dc.identifier.urihttps://hdl.handle.net/1911/117538en_US
dc.language.isoengen_US
dc.publisherMDPIen_US
dc.rightsExcept where otherwise noted, this work is licensed under a Creative Commons Attribution (CC BY) license.  Permission to reuse, publish, or reproduce the work beyond the terms of the license or beyond the bounds of fair use or other exemptions to copyright law must be obtained from the copyright holder.en_US
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/en_US
dc.titleSiONx Coating Regulates Mesenchymal Stem Cell Antioxidant Capacity via Nuclear Erythroid Factor 2 Activity under Toxic Oxidative Stress Conditionsen_US
dc.typeJournal articleen_US
dc.type.dcmiTexten_US
dc.type.publicationpublisher versionen_US
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