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ABSTRACT:
PROVIDER: PRJNA1289895 | ENA |
REPOSITORIES: ENA
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Project description:This study aimed to characterize the miRNA expression profile of plasma-derived small extracellular vesicles (sEVs) from diabetic foot rats treated with tibial cortex transverse transport. Plasma sEVs were isolated from peripheral blood samples of diabetic foot rats treated with either tibial transverse transport or sham surgery, followed by small RNA sequencing. Differentially expressed miRNAs were analyzed to explore the potential regulatory mechanisms by which tibial transverse transport promotes diabetic wound repair, with particular focus on angiogenesis, inflammatory regulation, immune modulation, and tissue regeneration.
2026-07-04 | GSE337487 | GEO
Project description:Impaired healing of diabetic wounds causes significant morbidity and mortality. This study aimed to identify novel mechanisms of diabetic wound healing defects and test a therapeutic intervention using diabetic mouse and pig models. We found Smad7 transgene expression in mouse epidermis promoting wound healing in diabetic dbdb mice, with reductions in obesity and blood glucose. To isolate effects of Smad7 on wounds, we created a Smad7-based biologic (Tat-PYC-Smad7) that penetrates wound cells. Topical application of Tat-PYC-Smad7 to diabetic pig and mouse wounds accelerated healing compared to controls. RNAseq analysis of mouse wound samples showed reduced TGF/NFB signaling, leading to faster re-epithelialization and better extracellular matrix remodeling. Tat-PYC-Smad7 also attenuated neutrophil degranulation and NETosis by blocking histone 3 citrullination and inhibiting myeloperoxidase activities. Our study reveals that Tat-PYC-Smad7 promotes diabetic wound healing by targeting keratinocytes and neutrophils, providing insight into cellular mechanisms of diabetic wound healing defects targetable by Smad7-based therapy.
2024-08-07 | MSV000095545 | MassIVE
Project description:MicroRNAs are powerful gene expression regulators, but their corneal repertoire and potential changes in corneal diseases remain unknown. Our purpose was to identify miRNAs altered in the human diabetic cornea by microarray analysis, and to examine their effects on wound healing in cultured telomerase-immortalized human corneal epithelial cells (HCEC) in vitro. Using microarrays, 29 miRNAs were identified as differentially expressed in diabetic samples. Two miRNA candidates showing the highest fold increased in expression in the diabetic cornea were confirmed by Q-PCR and further characterized. HCEC transfection with h-miR-146a or h-miR-424 significantly retarded wound closure, but their respective antagomirs significantly enhanced wound healing vs. controls. Cells treated with h-miR-146a or h-miR-424 had decreased p-p38 and p-EGFR staining, but these increased over control levels close to the wound edge upon antagomir treatment. In conclusion, several miRNAs with increased expression in human diabetic central corneas were found. Two such miRNAs inhibited cultured corneal epithelial cell wound healing. Dysregulation of miRNA expression in human diabetic cornea may be an important mediator of abnormal wound healing.
2013-11-09 | GSE52233 | GEO
Project description:Purpose: To characterize exosomes derived from a mouse corneal progenitor cell line and investigate their role in delayed wound healing and sensory neuropathy in diabetic corneas. Methods: TKE2 cells were cultured in normal glucose (NG, 5 mM) or high glucose (HG, 25 mM) media for three passages. At passage 4, confluent cultures with or without scratch wounding were collected at 8 and 96 h. Exosomes were isolated by centrifugation and filtration and characterized by nanoparticle tracking analysis, cryo-TEM, and Western blotting. Their functions were tested by applying exosomes to unwounded and wounded corneas. The purified exosomes were analyzed by LC-MS/MS proteomics. The role of two identified proteins, HTRA1 and STAT3, in epithelial wound closure was assessed by siRNA and small molecular inhibitor, respectively. Results: The isolated extracellular vesicles were confirmed as exosomes, which were taken up by corneal epithelial cells and sensory nerves. While there were no effects on epithelial wound closure of NL corneas, exosomes from healing, but not quiescent, TKE2 cells accelerated delayed wound closure in DM corneas. In wounded corneas, siRNA knockdown of HTRA1—an abundant protein in healing TKE2 exosomes—impaired wound healing in normal but not diabetic corneas, while inhibition of exosomal Stat3 partially reduced the capacity of healing TK2 exosomes in promoting epithelial wound closure in DM corneas. Conclusions: Exosomes secreted by corneal epithelial progenitor cells exert distinct functions depending on culture conditions. Modulating exosomal contents may represent a therapeutic strategy to enhance wound healing in diabetic corneas.
2026-09-16 | PXD074015 | Pride
Project description:MicroRNAs are powerful gene expression regulators, but their corneal repertoire and potential changes in corneal diseases remain unknown. Our purpose was to identify miRNAs altered in the human diabetic cornea by microarray analysis, and to examine their effects on wound healing in cultured telomerase-immortalized human corneal epithelial cells (HCEC) in vitro. Using microarrays, 29 miRNAs were identified as differentially expressed in diabetic samples. Two miRNA candidates showing the highest fold increased in expression in the diabetic cornea were confirmed by Q-PCR and further characterized. HCEC transfection with h-miR-146a or h-miR-424 significantly retarded wound closure, but their respective antagomirs significantly enhanced wound healing vs. controls. Cells treated with h-miR-146a or h-miR-424 had decreased p-p38 and p-EGFR staining, but these increased over control levels close to the wound edge upon antagomir treatment. In conclusion, several miRNAs with increased expression in human diabetic central corneas were found. Two such miRNAs inhibited cultured corneal epithelial cell wound healing. Dysregulation of miRNA expression in human diabetic cornea may be an important mediator of abnormal wound healing. Total RNA was extracted from age-matched human autopsy normal (n=6) and diabetic (n=6) central corneas, Flash Tag end-labeled, and hybridized to Affymetrix® GeneChip® miRNA Arrays. Select miRNAs associated with diabetic cornea were validated by quantitative RT-PCR (Q-PCR) and by in situ hybridization (ISH) in independent samples.
2013-11-09 | E-GEOD-52233 | biostudies-arrayexpress
Project description:Impaired wound healing is one of the main reasons that leads to diabetic foot ulcerations. However, the exact mechanism of delayed wound healing in diabetes mellitus is not fully understood. Long non-coding RNAs (lncRNAs) are widely involved in a variety of biological processes and diseases, including diabetes and its associated complications. To further identify the roles of LncRNAs in diabetic wound healing, four STZ induced diabetic rat skin tissues and four control rat skin tissues were prepared for a LncRNAs microarray expression profiling by using rat LncRNA Array (4 x 44K, Arraystar).
2022-09-29 | GSE214338 | GEO
Project description:Background: Diabetic wounds are a major complication of diabetes mellitus and heal poorly due to persistent inflammation, fibroblast dysfunction, oxidative stress, mitochondrial injury, and impaired angiogenesis. Scutellarein (SCU) is a natural flavonoid with demonstrated anti-inflammatory, antioxidant, and fibroblast-relevant bioactivities, but its effects on diabetic wound repair and the underlying molecular mechanisms remain poorly defined. Methods: A streptozotocin-induced diabetic mouse cutaneous wound model was used to evaluate the effects of topical SCU treatment on wound closure, epithelial repair, and collagen deposition. In vitro, an H₂O₂-induced oxidative injury model in fibroblasts was employed to assess SCU-mediated protection on migration, viability, redox balance, and mitochondrial structure and function. Transcriptomics (RNA-seq) was performed to identify SCU-responsive molecular pathways, and SCU-P2RX1 molecular docking combined with ATP rescue experiments was used to interrogate a P2RX1–calcium axis. Results: SCU accelerated diabetic wound closure and improved epithelial gap, collagen deposition, fibroblast-like cell proliferation, and angiogenesis in vivo. In vitro, SCU promoted fibroblast migration, suppressed H₂O₂-induced cell death, reduced intracellular ROS, restored mitochondrial morphology and membrane potential, and preserved ATP production. RNA-seq revealed that SCU downregulated P2rx1 and enriched calcium-transport, mitochondrial, and wound-healing pathways. Molecular docking predicted SCU binding to P2RX1 with a docking score of ΔG = −9.2 kcal/mol, and ATP addition reversed the SCU-mediated suppression of calcium overload, mitochondrial depolarization, and inflammatory gene expression.
2026-06-02 | GSE333609 | GEO
Project description:Impaired healing of diabetic wounds causes significant morbidity and mortality. This study aimed to identify novel mechanisms of diabetic wound healing defects and test a therapeutic intervention using diabetic mouse and pig models. We found Smad7 transgene expression in mouse epidermis promoting wound healing in diabetic db/db mice, with reductions in obesity and blood glucose. To isolate effects of Smad7 on wounds, we created a Smad7-based biologic (Tat-PYC-Smad7) that penetrates wound cells. Topical application of Tat-PYC-Smad7 to diabetic pig and mouse wounds accelerated healing compared to controls. RNAseq analysis of mouse wound samples showed reduced TGFβ/NFκB signaling, leading to faster re-epithelialization and better extracellular matrix remodeling. Tat-PYC-Smad7 also attenuated neutrophil degranulation and NETosis by blocking histone 3 citrullination and inhibiting myeloperoxidase activities. Our study reveals that Tat-PYC-Smad7 promotes diabetic wound healing by targeting keratinocytes and neutrophils, providing insight into cellular mechanisms of diabetic wound healing defects targetable by Smad7-based therapy.
2024-08-13 | GSE274513 | GEO
Project description:Diabetic chronic wounds exhibit impaired tissue repair characterized by persistent inflammation, oxidative stress, defective extracellular matrix remodeling, and insufficient regeneration. In this study, RNA sequencing was performed to investigate transcriptomic changes in diabetic wound tissues following treatment with multifunctional microneedles (DST-MNs) integrating spermidine- and TGF-β3-regulated dental pulp stem cell spheroids. Full-thickness diabetic wounds were established in rats, and wound tissues from untreated diabetic wound animals and DST-MNs-treated animals were collected for transcriptome profiling. Differentially expressed genes and enriched biological pathways were analyzed to identify molecular mechanisms associated with DST-MNs-mediated wound repair. These data provide insights into transcriptional regulation involved in inflammatory modulation, extracellular matrix remodeling, angiogenesis, and diabetic wound regeneration.
2026-08-11 | GSE342853 | GEO
Project description:At present, there is no effective treatment for diabetic wounds, and the cost of treatment is high. MicroRNAs (miRNAs) plays an important role in the process of diabetic wound healing. By regulating the expression of target genes, it regulates growth factors, cytokines and signal pathways, thereby affecting various stages of ulcer healing such as hemostasis, anti-inflammatory, proliferation and remodeling. In this study, differential expression of miRNAs in diabetic wound was screened. MiR-206 was selected as the research object to detect the effect of miR-206 on the proliferation of fibroblasts and vascular endothelial cell by regulating HIF-1?. Finally, in vivo studies showed that miR-206 antagomir could promote the expression of HIF-1?, CD34 and VEGF, and further promote wound healing in diabetic rats.
2022-11-10 | GSE188783 | GEO