Journal article
Extracellular biomolecular free radical formation during injury
Free radical biology & medicine, Vol.188, pp.175-184
06/17/2022
DOI: 10.1016/j.freeradbiomed.2022.06.223
PMCID: PMC9725094
PMID: 35724853
Abstract
Determine if oxidative damage increases in articular cartilage as a result of injury and matrix failure and whether modulation of the local redox environment influences this damage.
Osteoarthritis is an age associated disease with no current disease modifying approaches available. Mechanisms of cartilage damage in vitro suggest tissue free radical production could be critical to early degeneration, but these mechanisms have not been described in intact tissue. To assess free radical production as a result of traumatic injury, we measured biomolecular free radical generation via immuno-spin trapping (IST) of protein/proteoglycan/lipid free radicals after a 2 J/cm2 impact to swine articular cartilage explants. This technique allows visualization of free radical formation upon a wide variety of molecules using formalin-fixed, paraffin-embedded approaches. Scoring of extracellular staining by trained, blinded scorers demonstrated significant increases with impact injury, particularly at sites of cartilage cracking. Increases remain in the absence of live chondrocytes but are diminished, thus appear to be a cell-dependent and -independent feature of injury. We then modulated the extracellular environment with a pulse of heparin to demonstrate the responsiveness of the IST signal to changes in cartilage biology. Addition of heparin caused a distinct change in the distribution of protein/lipid free radicals at sites of failure alongside a variety of pertinent redox changes related to osteoarthritis. This study directly confirms the production of biomolecular free radicals from articular trauma, providing a rigorous characterization of their formation by injury.
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•Impact injury to articular cartilage causes biomolecular free radical production at sites of cartilage cracking.•This free radical production is a result of cell dependent and independent factors.•Manipulation of the extracellular redox environment to mimic diseased tissue results in concentration of this radical damage at the site of the crack.
Details
- Title: Subtitle
- Extracellular biomolecular free radical formation during injury
- Creators
- Madeline R. Hines - University of IowaJessica E. Goetz - University of IowaPiedad C. Gomez-Contreras - University of IowaSamuel N. Rodman - University of IowaSuryamin Liman - The University of Iowa, Iowa City, IA, USAElise L. Femino - The University of Iowa, Iowa City, IA, USAPaige N. Kluz - University of Wisconsin–MadisonBrett A. Wagner - University of IowaGarry R. Buettner - University of IowaEric E. Kelley - West Virginia UniversityMitchell C. Coleman - The University of Iowa, Iowa City, IA, USA
- Resource Type
- Journal article
- Publication Details
- Free radical biology & medicine, Vol.188, pp.175-184
- DOI
- 10.1016/j.freeradbiomed.2022.06.223
- PMID
- 35724853
- PMCID
- PMC9725094
- NLM abbreviation
- Free Radic Biol Med
- ISSN
- 0891-5849
- eISSN
- 1873-4596
- Publisher
- Elsevier Inc
- Language
- English
- Date published
- 06/17/2022
- Academic Unit
- Roy J. Carver Department of Biomedical Engineering; Orthopedics and Rehabilitation; Radiation Oncology
- Record Identifier
- 9984269360002771
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