No abstract

Autophagy is critical for recycling amino acids and nitrogenrich nucleotides, adjusting respiratory substrates, and the retention of assimilated nitrogen during fixed-carbon starvation.

Background: Negative pressure wound therapy (NPWT) is an option for securing meshed split thickness skin grafts (mSTSGs) after burn excision to optimize skin graft adherence.Recently, the use of autologous skin cell suspension (ASCS) has been approved for use in the treatment of burn injuries in conjunction with mSTSGs.To date, limited data exists regarding the impact of NPWT on healing outcomes when the cellular suspension is utilized. It was hypothesized that NPWT would not negatively impact wound healing of ASCS + mSTSG. Materials and Methods:A burn, excision, mSTSG, ASCS ± NPWT model was used. Two Duroc pigs were utilized in this experiment, each with 2 sets of paired burns. Four wounds received mSTSG + ASCS + NPWT through post-operative day 3, and 4 wounds received mSTSG + ACSC + traditional ASCS dressings. Cellular viability was characterized prior to spraying. Percent reepithelialization, graft-adherence, pigmentation, elasticity, and blood perfusion and blood vessel density were assessed at multiple time points through 2 weeks.Results: All wounds healed within 14 days with minimal scar pathology and no significant differences in percent re-epithelialization between NPWT, and non-NPWT wounds were observed. Additionally, no differences were detected for pigmentation, perfusion, or blood ves-✩ This work was funded by AVITA Medical. The NWPT devices were obtained as a donation from KCI. Dr. Shupp is a consultant for AVITA Medical.

No abstract

Upon healing, burn wounds often leave hypertrophic scars (HTSs) marked by excess collagen deposition, dermal and epidermal thickening, hypervascularity, and an increased density of fibroblasts. The Galectins, a family of lectins with a conserved carbohydrate recognition domain, function intracellularly and extracellularly to mediate a multitude of biological processes including inflammatory responses, angiogenesis, cell migration and differentiation, and cell‐ECM adhesion. Galectin‐1 (Gal‐1) has been associated with several fibrotic diseases and can induce keratinocyte and fibroblast proliferation, migration, and differentiation into fibroproliferative myofibroblasts. In this study, Gal‐1 expression was assessed in human and porcine HTS. In a microarray, galectins 1, 4, and 12 were upregulated in pig HTS compared to normal skin (fold change = +3.58, +6.11, and +3.03, FDR <0.01). Confirmatory qRT‐PCR demonstrated significant upregulation of Galectin‐1 (LGALS1) transcription in HTS in both human and porcine tissues (fold change = +7.78 and +7.90, P <.05). In pig HTS, this upregulation was maintained throughout scar development and remodeling. Immunofluorescent staining of Gal‐1 in human and porcine HTS showed significantly increased fluorescence (202.5 ± 58.2 vs 35.2 ± 21.0, P <.05 and 276.1 ± 12.7 vs 69.7 ± 25.9, P <.01) compared to normal skin and co‐localization with smooth muscle actin‐expressing myofibroblasts. A strong positive correlation (R = .948) was observed between LGALS1 and Collagen type 1 alpha 1 mRNA expression. Gal‐1 is overexpressed in HTS at the mRNA and protein levels and may have a role in the development of scar phenotypes due to fibroblast over‐proliferation, collagen secretion, and dermal thickening. The role of galectins shows promise for future study and may lead to the development of a pharmacotherapy for treatment of HTS.