The repairing role of phycocyanin from Spirulina in chronic refractory wound healing and mechanism analysis
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PROVIDER: PRJNA1258300 | ENA |
REPOSITORIES: ENA
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Project description:This study aimed to explore the therapeutic potential of cyano-phycocyanin (C-PC) to improve the efficiency of chronic refractory wound healing processes. The hormone induced chronic refractory skin ulcer model were established on the backs of mice. Assessment of wound-healing efficiency of C-PC was evaluated by analyzing total wound closure, recovery percentage and epidermal thickness of wounds. Hematoxylin-eosin, Masson trichrome and immunohistochemical analysis were performed to evaluate the re-epithelialization, inflammatory response, granulation tissue formation and fibrotic tissue formation. Differentially expressed genes were identified through RNA-seq, polymerase chain reaction (PCR) array and confirmed by quantitative PCR (qPCR). Cell viability was determined using a cell counting kit-8 (CCK-8) assay, migration and angiogenesis were detected by wound healing and tube formation assays. The related protein expression was analyzed by Western blot. The results demonstrated a significantly higher wound-healing rate in C-PC group compared to the control group at 3, 7, 14, and 21 days (p< 0.05). The mechanism may involve increased collagen accumulation, promotion of angiogenesis and reduction in the infiltration of inflammatory cells. Additionally, VEGFR-2 was highly likely to be the target for C-PC. Thus, C-PC may hold potential for the treatment of wound healing and ischemic/ reperfusion injuries.
2025-06-01 | GSE296266 | GEO
Project description:Wound healing is a dynamic and complex process. The proliferation and migration of dermal fibroblasts are crucial for wound healing. Recent studies have indicated that the extracts from Spirulina platensis have a positive potential for wound healing. However, its underlying mechanism is not fully understood. Our previous study showed that spirulina crude protein (SPCP) promoted the viability of human dermal fibroblast cell line (CCD-986sk cells). In this study, we further investigated the wound healing effect and corresponding mechanisms of SPCP on CCD-986sk cells. Bromodeoxyuridine (BrdU) assay showed that SPCP promoted the proliferation of CCD-986sk cells. The wound healing assay showed that SPCP promoted the migration of CCD-986sk cells. Furthermore, cell cycle analysis demonstrated that SPCP promoted CCD-986sk cells to enter S and G₂/M phases from G₀/G₁ phase. Western blot results showed that SPCP significantly upregulated the expression of cyclin D1, cyclin E, cyclin-dependent kinase 2 (Cdk2), cyclin-dependent kinase 4 (Cdk4), and cyclin-dependent kinase 6 (Cdk6), as well as inhibited the expression of CDK inhibitors p21 and p27 in CCD-986sk cells. In the meanwhile, SPCP promoted the phosphorylation and activation of phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt). However, the phosphorylation of Akt was significantly blocked by PI3K inhibitor (LY294002), which in turn reduced the SPCP-induced proliferation and migration of CCD-986sk cells. Therefore, the results presenting in this study suggested that SPCP can promote the proliferation and migration of CCD-986sk cells; the PI3K/Akt signaling pathway play a positive and important role in these processes.
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Project description:Impaired skin wound healing is a significant global health issue, especially among the elderly. Wound healing is a well-orchestrated process involving the sequential phases of inflammation, proliferation, and tissue remodeling. Although wound healing is a highly dynamic and energy-requiring process, the role of metabolism remains largely unexplored. By combining transcriptomics and metabolomics of human skin biopsy samples, we mapped the core bioenergetic and metabolic changes in normal acute as well as chronic wounds in elderly subjects. We found upregulation of glycolysis, the tricarboxylic acid cycle, glutaminolysis, and β-oxidation in the later stages of acute wound healing and in chronic wounds. To ascertain the role of these metabolic pathways on wound healing, we targeted each pathway in a wound healing assay as well as in a human skin explant model using metabolic inhibitors and stimulants. Enhancement or inhibition of glycolysis and, to a lesser extent, glutaminolysis had a far greater impact on wound healing than similar manipulations of oxidative phosphorylation and fatty acid β-oxidation. These findings increase the understanding of wound metabolism and identify glycolysis and glutaminolysis as potential targets for therapeutic intervention.
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Project description:In order to clarify the human response of re-epithelialization, we biopsied split-thickness skin graft donor site wounds immediately before and after harvesting, as well as during the healing process 3 and 7 days thereafter. Altogether 25 biopsies from 8 patients qualified for the study. All samples were analysed by genome-wide microarrays. Here we identified the genes associated with normal skin re-epithelialization on time-scale, and organized them by similarities according to their induction or suppression patterns during wound healing. Overall 25 samples were analyzed
2011-04-29 | E-GEOD-28914 | biostudies-arrayexpress
Project description:The process of wound healing in humans is poorly understood. To identify spatiotemporal gene expression patterns during human wound healing, we performed single cell and spatial transcriptomics profiling of human in vivo wound samples.
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