
Stephanie J. Bryant
· Associate Professor (Chemical and Biological Engineering)VerifiedUniversity of Colorado Boulder · Molecular, Cellular & Developmental Biology
Active 1999–2026
About
Stephanie J. Bryant is a Professor in the Department of Chemical and Biological Engineering, the BioFrontiers Institute, and the Material Science and Engineering Program at the University of Colorado at Boulder. She directs the Bryant Research Group, which is part of the Biomaterials and Functional Tissue Engineering Laboratory. Her research program lies at the interface of engineering, material science, and biology, focusing on addressing key biological questions and developing new strategies for tissue engineering.
Research topics
- Computer Science
- Materials science
- Biology
- Engineering
- Artificial Intelligence
- Biomedical engineering
- Nanotechnology
- Biological system
- Chemical engineering
- Cell biology
- Biochemical engineering
- Chemistry
- Anatomy
- Composite material
- Polymer chemistry
Selected publications
The Effects of TGFβ3 Presentation on Chondrogenesis in a Cartilage-mimetic Hydrogel
SSRN Electronic Journal · 2026-01-01
preprintOpen accessSenior authorSSRN Electronic Journal · 2025-01-01
preprintOpen accessThe foreign body response to biomaterial implants is reduced by co-inhibition of TLR2 and TLR4
Acta Biomaterialia · 2025-06-12 · 3 citations
articleOpen accessSenior authorCorrespondingACS Biomaterials Science & Engineering · 2025-06-12 · 1 citations
articleOpen accessSenior authorCorrespondingPoly(ethylene glycol) hydrogels prepared from PEG diacrylate (PEGDA) monomers are widely investigated for biological applications including drug delivery and tissue engineering. Despite their high-water contents, PEGDA hydrogels when implanted into the body induce a foreign body response (FBR). The overall goal of this study was to investigate the role of surface adsorbed proteins in the FBR to PEGDA hydrogels and determine whether they act as damage associated molecular patterns (DAMPs) to initiate inflammation. Toll-like receptors (TLRs) 2 and 4 are one of the primary receptors that recognize DAMPs. In vitro and in vivo studies were performed using wildtype (Wt), TLR2–/–, TLR4–/–, and TLR2–/–TLR4–/– double knockout (DKO) mice. In vitro, Wt neutrophils were activated in response to the PEGDA hydrogels as measured by myeloperoxidase, and this response was partially mediated by TLR4 but not TLR2. Wt macrophages predisposed to an inflammatory state responded to the PEGDA hydrogel itself and to a greater extent to surface-adsorbed plasma by producing the pro-inflammatory cytokines interleukin 6 and tumor necrosis factor α. TLR4 and to a lesser extent TLR2 mediated this response. To link DAMPs to the FBR in vivo, PEGDA hydrogels were implanted subcutaneously in mice. The thickness of the inflammatory cell layer was mediated by both TLR2 and TLR4 as knocking out both TLRs led to significantly fewer inflammatory cells. The fibrous capsule was reduced by 50% in both single KO mice as well as the DKO mice. Taken together, this study determined that DAMPs formed from surface-adsorbed plasma activate TLR4. In the more complex in vivo environment, both TLR2 and TLR4 are major contributors to the inflammatory response and partial contributors to the fibrous encapsulation. Overall, these findings provide a critical link between DAMPs, TLRs, immune cells, and the FBR to PEGDA hydrogels.
Annals of Biomedical Engineering · 2024-04-29 · 18 citations
articleOpen accessACS Biomaterials Science & Engineering · 2024-02-06 · 9 citations
articleOpen accessSenior authorCorrespondingProtein adsorption after biomaterial implantation is the first stage of the foreign body response (FBR). However, the source(s) of the adsorbed proteins that lead to damaged associated molecular patterns (DAMPs) and induce inflammation have not been fully elucidated. This study examined the effects of different protein sources, cell-derived (from a NIH/3T3 fibroblast cell lysate) and serum-derived (from fetal bovine serum), which were compared to implant-derived proteins (after a 30 min subcutaneous implantation in mice) on activation of RAW 264.7 cells cultured in minimal (serum-free) medium. Both cell-derived and serum-derived protein sources when preadsorbed to either tissue culture polystyrene or medical-grade silicone induced RAW 264.7 cell activation. The combination led to an even higher expression of pro-inflammatory cytokine genes and proteins. Implant-derived proteins on silicone explants induced a rapid inflammatory response that then subsided more quickly and to a greater extent than the studies with in vitro cell-derived or serum-derived protein sources. Proteomic analysis of the implant-derived proteins identified proteins that included cell-derived and serum-derived, but also other proteinaceous sources (e.g., extracellular matrix), suggesting that the latter or nonproteinaceous sources may help to temper the inflammatory response in vivo. These findings indicate that both serum-derived and cell-derived proteins adsorbed to implants can act as DAMPs to drive inflammation in the FBR, but other protein sources may play an important role in controlling inflammation.
Molecular Therapy · 2024-05-03 · 3 citations
articleOpen accessACS Applied Bio Materials · 2023-06-27 · 6 citations
articleSenior authorCorrespondingMatrix metalloproteinase (MMP)-sensitive hydrogels are promising for cartilage tissue engineering due to cell-mediated control over hydrogel degradation. However, any variability in MMP, tissue inhibitors of matrix metalloproteinase (TIMP), and/or extracellular matrix (ECM) production among donors will impact neotissue formation in the hydrogels. The goal for this study was to investigate the impact of inter- and intra-donor variability on the hydrogel-to-tissue transition. Transforming growth factor β3 was tethered into the hydrogel to maintain the chondrogenic phenotype and support neocartilage production, allowing the use of chemically defined medium. Bovine chondrocytes were isolated from two donor groups, skeletally immature juvenile and skeletally mature adult donors (inter-donor variability) and three donors within each group (intra-donor group variability). While the hydrogel supported neocartilaginous growth by all donors, donor age impacted MMP, TIMP, and ECM synthesis rates. Of the MMPs and TIMPs studied, MMP-1 and TIMP-1 were the most abundantly produced by all donors. Adult chondrocytes secreted higher levels of MMPs, which was accompanied by higher production of TIMPs. Juvenile chondrocytes exhibited more rapid ECM growth. By day 29, juvenile chondrocytes had surpassed the gel-to-tissue transition. On the contrary, the adult donors had a percolated polymer network indicating that despite higher levels of MMPs the gel-to-transition had not yet been achieved. The intra-donor group variability of MMP, TIMP, and ECM production was higher in adult chondrocytes but did not impact the extent of the gel-to-tissue transition. In summary, age-dependent inter-donor variations in MMPs and TIMPs significantly impact the timing of the gel-to-tissue transition in MMP-sensitive hydrogels.
Acta Biomaterialia · 2023-08-25 · 16 citations
articleOpen accessSenior authorCorrespondingSSRN Electronic Journal · 2023-01-01
preprintOpen accessSenior author
Recent grants
NIH · $1.5M · 2019
NIH · $365k · 2015
NIH · $156k · 2019
NIH · $231k · 2013
NIH · $358k · 2017
Frequent coauthors
- 38 shared
Kristi S. Anseth
University of Colorado Boulder
- 23 shared
Virginia L. Ferguson
University of Colorado Boulder
- 21 shared
Franck J. Vernerey
University of Colorado Boulder
- 18 shared
Elizabeth A. Aisenbrey
University of Wisconsin–Madison
- 16 shared
Robert R. McLeod
- 14 shared
Karin A. Payne
University of Colorado Anschutz Medical Campus
- 13 shared
Mark A. Randolph
Massachusetts General Hospital
- 13 shared
Justine J. Roberts
W. L. Gore & Associates (United States)
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