SDF-1α gene-activated collagen scaffold drives functional differentiation of human Schwann cells for wound healing applications

Enhancing angiogenesis is the prime target of current biomaterial-based wound healing strategies. However, these approaches largely overlook the angiogenic role of the cells of the nervous system. Therefore, we explored the role of a collagen-chondroitin sulfate scaffold functionalized with a proangiogenic gene stromal-derived factor-1α (SDF-1α)—an SDF-1α gene-activated scaffold on the functional regulation of human Schwann cells (SCs). A preliminary 2D study was conducted by delivering plasmids encoding for the SDF-1α gene into a monolayer of SCs using polyethyleneimine-based nanoparticles. The delivery of the SDF-1α gene into the SCs enhanced the production of proangiogenic vascular endothelial growth factor (VEGF). Subsequently, we investigated the impact of SDF-1α gene-activated scaffold (3D) on the SCs for 2 weeks, using a gene-free scaffold as control. The transfection of the SCs within the gene-activated scaffold resulted in transient overexpression of SDF-1α transcripts and triggered the production of bioactive VEGF that enhanced endothelial angiogenesis. The overexpression of SDF-1α also caused transient activation of the transcription factor c-Jun and supported the differentiation of SCs towards a repair phenotype. This was characterized by elevated expression of neurotrophin receptor p75NGFR. During this developmental stage, the SCs also performed an extensive remodelling of the basement matrix (fibronectin, collagen IV, and laminin) to enrich their environment with the pro-neurogenic matrix protein laminin, revealing an enhanced pro-neurogenic behavior. Together, this study shows that SDF-1α gene-activated scaffold is a highly bioinstructive scaffold capable of enhancing proangiogenic regenerative response in human SCs for improved wound healing

Gum Arabic supplementation prevents loss of learning and memory through stimulation of mitochondrial function in the hippocampus of type 2 diabetic rats

The aim was to determine whether gum Arabic (GA) supplementation prevents cognitive decline in type 2 diabetes, through stimulation of mitochondrial function in the hippocampus. Type 2 diabetic rats and controls were assigned to following groups for 16 weeks: Control + Water; Control + GA 10% w/v; Diabetes + Water; Diabetes + GA 10% w/v. Latency in water maze was shorter for Diabetes + GA compared to Diabetes + Water (P < 0.05). Diabetes + GA group had a higher expression density per cell of peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) compared to Diabetes + Water (P < 0.05). A similar trend was observed for ATP synthase β-subunit expression (ATPB). Number of PGC-1α positive cells was higher in diabetes compared to control groups (p < 0.05). The GA prevented learning and memory loss in type 2 diabetes. This was associated with greater expression of PGC-1a and a trend for greater ATBP protein expression in the hippocampus