ArticlePloS one2013
Wound healing improvement with PHD-2 silenced fibroblasts in diabetic mice.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- Fibroblast-Based Cell Therapy: Molecular Background, Current Therapies and Future Perspectives.Cells · 2026Review
- Modulating the extracellular matrix to treat wound healing defects in Ehlers-Danlos syndrome.iScience · 2024Article
- Use of Therapeutic RNAs to Accelerate Wound Healing in Diabetic Rabbit Wounds.Advances in wound care · 2024Article
- Small interfering RNA (siRNA) as a potential gene silencing strategy for diabetes and associated complications: challenges and future perspectives.Journal of diabetes and metabolic disorders · 2024Review
- Targeting Signalling Pathways in Chronic Wound Healing.International journal of molecular sciences · 2023Review
- Gene therapy to enhance angiogenesis in chronic wounds.Molecular therapy. Nucleic acids · 2022Review
- HIF1A promotes miR-210/miR-424 transcription to modulate the angiogenesis in HUVECs and HDMECs via sFLT1 under hypoxic stress.Molecular and cellular biochemistry · 2022Article
- Possible roles of anti-type II collagen antibody and innate immunity in the development and progression of diabetic retinopathy.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2022Review
- The Emerging Role of Immune Cells and Targeted Therapeutic Strategies in Diabetic Wounds Healing.Journal of inflammation research · 2022Review
- Approaches to Modulate the Chronic Wound Environment Using Localized Nucleic Acid Delivery.Advances in wound care · 2021Review
- HIF1α/miR-199a/ADM feedback loop modulates the proliferation of human dermal microvascular endothelial cells (HDMECs) under hypoxic condition.Cell cycle (Georgetown, Tex.) · 2019Article
- Von Hippel-Lindau (VHL) Protein Antagonist VH298 Improves Wound Healing in Streptozotocin-Induced Hyperglycaemic Rats by Activating Hypoxia-Inducible Factor- (HIF-) 1 Signalling.Journal of diabetes research · 2019Article
- Acceleration of Diabetic Wound Healing with PHD2- and miR-210-Targeting Oligonucleotides.Tissue engineering. Part A · 2019Article
- PHD-2 Suppression in Mesenchymal Stromal Cells Enhances Wound Healing.Plastic and reconstructive surgery · 2018Article
- A Cooperative Copper Metal-Organic Framework-Hydrogel System Improves Wound Healing in Diabetes.Advanced functional materials · 2017Article
- Local Delivery of PHD2 siRNA from ROS-Degradable Scaffolds to Promote Diabetic Wound Healing.Advanced healthcare materials · 2016Article
- Prolyl hydroxylase 2 (PHD2) inhibition protects human renal epithelial cells and mice kidney from hypoxia injury.Oncotarget · 2016Article
- Iron-chelating agent desferrioxamine stimulates formation of neutrophil extracellular traps (NETs) in human blood-derived neutrophils.Bioscience reports · 2016Article
- PHD2: from hypoxia regulation to disease progression.Hypoxia (Auckland, N.Z.) · 2016Review
- Short Hairpin RNA Silencing of PHD-2 Improves Neovascularization and Functional Outcomes in Diabetic Wounds and Ischemic Limbs.PloS one · 2016Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHypoxia-inducible factor 1α is the central regulator of the hypoxia-induced response which results in the up-regulation of angiogenic factors. Its activity is under precise regulation of prolyl-hydroxylase domain 2. We hypothesized that PHD2 silenced fibroblasts would increase the expression of angiogenic factors, which might contribute to the improvement of the diabetic wound healing. MATERIALS AND
methods50 dB/db mice were employed and randomly assigned into five groups with 10 mice in each: group 1 (untreated cell), group 2 (PHD2 silenced cell), group 3 (L-mimosine treated cells), group 4 (nontargeting siRNA treated cells) and group 5 (sham control). Fibroblasts were cultivated from the dermis of mice in each group and treated with PHD2 targeting siRNA, L-mimosine and non-targeting siRNA respectively. A fraction of the fibroblasts were employed to verify the silencing rate of PHD2 after 48 hours. The autologous fibroblasts (treated and untreated) labeled with adenovirus-GFP were implanted around the wound (Φ6mm), which was created on the dorsum of each mouse. The status of wounds was recorded periodically. Ten days postoperatively, 3 mice from each group were sacrificed and wound tissues were harvested. Molecular biological examinations were performed to evaluate the expressions of cytokines. 28 days postoperatively, the remaining mice were sacrificed. Histological examinations were performed to evaluate the densities of GFP+ cells and capillaries.
resultsThe expression of PHD2 reduced to 12.5%, and the expressions of HIF-1α and VEGFa increased significantly after PHD2 siRNA treatment. With the increasing expressions of HIF-1α and VEGFa, the time to wound closure in group 2 was less than 2 weeks. Increased numbers of GFP+ cells and capillaries were observed in group 2.
conclusionPHD2 siRNA treatment not only increased the expression of HIF1α and VEGFa, but also improved the fibroblast proliferation. These effects might contribute to the improvement of the diabetic wound healing.
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