Poly(ethylene glycol)-b-poly(L-alanine) (PEG-L-PA)s with L-PA molecular weights of 620, 1100, and 2480 Da and a fixed molecular weight of PEG at 5000 Da were synthesized to compare the thermosensitive behavior, and to investigate their potential as a three-dimensional (3D) culture matrix of adipose-tissue-derived stem cells (ADSCs). The sol-to-gel transition temperature and the concentration ranges where the transition was observed decreased as the L-PA molecular weight increased. ADSCs were cultured in the 3D matrixes of in situ formed PEG-L-PA hydrogels, which were produced by increasing the temperature of cell-suspended PEG-L-PA aqueous solutions. The spherical morphology was maintained in the PEG-L-PA hydrogel, while the cells underwent fibroblastic morphological changes in the Matrigel over 14 days of incubation. ADSCs exhibited high expression of type II collagen in the PEG-L-PA thermogel. In addition, they also moderately expressed the biomarker of myogenic differentiation factor 1 as the same mesodermal lineages, as well as the type III β-tubulin as a cross-differentiation biomarker. Similar to the in vitro study, the ADSCs predominantly exhibited chondrogenic biomarkers in the in vivo study. The study demonstrates that the polypeptide thermogel of PEG-L-PA is promising as a 3D culture matrix of ADSCs and as an injectable tissue engineering biomaterial.

PRP treatment improved the survival and quality of fat grafts. Safer methods of PRP activation and preparation should be further investigated for potential application in humans.

This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .

No abstract

Background: Ischemia-reperfusion (I/R) injury is a leading cause of surgical skin flap compromise and organ dysfunction. Platelet-rich plasma (PRP) is an abundant reserve of various growth factors. Activated platelets play a role in endothelial damage during I/R injury; however, exogenous PRP could inhibit the production of reactive oxygen species. The goal of this study was to investigate the effect of PRP on I/R injury. Methods: Four groups (n=30) of C57BL/6N mice with lateral thoracic artery island flaps were used. Group A, the control group, received flap elevation and repositioning. Group B received PRP and repositioning. Group C had 4 hours of ischemia and then were reperfused. Group D received PRP, had 4 hours of ischemia, and then were reperfused. The survival area of flap tissue and blood perfusion were assessed. Histological evaluation included neutrophil counts. Reactive oxygen species and proinflammatory cytokines were measured to evaluate I/R injury. Protein expression of phosphorylated apoptosis signaling regulating kinase-1 (pASK-1), p38MAPK, and pNF-κB was measured by western blot. Results: PRP treatment enhanced the survival area and perfusion of the flap, reduced neutrophil accumulation in mice subjected to I/R injury. PRP treatment also showed a protective effect, with decreases in nitric oxide, myeloperoxidase, malondialdehyde concentrations. Additionally, PRP suppresses monocyte chemotactic protein-1, TNF-α, IL-1β, and IL-6. Finally, PRP decreased ASK-1 and NF-κB expression in tissues with I/R injury. Conclusion: PRP acts as a protective factor during flap I/R injury by reducing reactive oxygen species level and proinflammatory cytokines via decreased expression of pASK-1 and pNF-κB.