ArticlePloS one2011
Modification of collagen by 3-deoxyglucosone alters wound healing through differential regulation of p38 MAP kinase.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 52 citations in OpenAlex.
- Article
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- External Application of Human Umbilical Cord-Derived Mesenchymal Stem Cells in Hyaluronic Acid Gel Repairs Foot Wounds of Types I and II Diabetic Rats Through Paracrine Action Mode.Stem cells translational medicine · 2023Article
- Flavonoids as Potential Wound-Healing Molecules: Emphasis on Pathways Perspective.International journal of molecular sciences · 2023Review
- Reversion of glucocorticoid-induced senescence and collagen synthesis decrease by LY294002 is mediated through p38 in skin.International journal of biological sciences · 2022Article
- TGF Beta Induces Vitamin D Receptor and Modulates Mitochondrial Activity of Human Pancreatic Cancer Cells.Cancers · 2021Article
- Sirt1-Mediated Anti-Aging Effects ofPreventive nutrition and food science · 2020Article
- Review
- Wound Healing Property of Curcuminoids as a Microcapsule-Incorporated Cream.Pharmaceutics · 2019Article
- Lupeol, a Pentacyclic Triterpene, Promotes Migration, Wound Closure, and Contractile Effect In Vitro: Possible Involvement of PI3K/Akt and p38/ERK/MAPK Pathways.Molecules (Basel, Switzerland) · 2018Article
- Interleukin-6 stimulates Akt and p38 MAPK phosphorylation and fibroblast migration in non-diabetic but not diabetic mice.PloS one · 2017Article
- Vitamin D regulating TGF-β induced epithelial-mesenchymal transition.Respiratory research · 2014Article
- Genome-wide DNA methylation analysis identifies a metabolic memory profile in patient-derived diabetic foot ulcer fibroblasts.Epigenetics · 2014Article
- MicroRNA-101 targets EZH2, MCL-1 and FOS to suppress proliferation, invasion and stem cell-like phenotype of aggressive endometrial cancer cells.Oncotarget · 2014Article
- Animal models of systemic sclerosis: their utility and limitations.Open access rheumatology : research and reviews · 2014Review
- ER stress-induced cell death mechanisms.Biochimica et biophysica acta · 2013Review
- Chemotaxis of human induced pluripotent stem cell-derived endothelial cells.American journal of translational research · 2013Article
- Glucose toxic effects on granulation tissue productive cells: the diabetics' impaired healing.BioMed research international · 2013Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWound healing is a highly dynamic process that requires signaling from the extracellular matrix to the fibroblasts for migration and proliferation, and closure of the wound. This rate of wound closure is impaired in diabetes, which may be due to the increased levels of the precursor for advanced glycation end products, 3-deoxyglucosone (3DG). Previous studies suggest a differential role for p38 mitogen-activated kinase (MAPK) during wound healing; whereby, p38 MAPK acts as a growth kinase during normal wound healing, but acts as a stress kinase during diabetic wound repair. Therefore, we investigated the signaling cross-talk by which p38 MAPK mediates wound healing in fibroblasts cultured on native collagen and 3DG-collagen. METHODOLOGY/PRINCIPAL
findingsUsing human dermal fibroblasts cultured on 3DG-collagen as a model of diabetic wounds, we demonstrated that p38 MAPK can promote either cell growth or cell death, and this was dependent on the activation of AKT and ERK1/2. Wound closure on native collagen was dependent on p38 MAPK phosphorylation of AKT and ERK1/2. Furthermore, proliferation and collagen production in fibroblasts cultured on native collagen was dependent on p38 MAPK regulation of AKT and ERK1/2. In contrast, 3DG-collagen decreased fibroblast migration, proliferation, and collagen expression through ERK1/2 and AKT downregulation via p38 MAPK. CONCLUSIONS/SIGNIFICANCE: Taken together, the present study shows that p38 MAPK is a key signaling molecule that plays a significantly opposite role during times of cellular growth and cellular stress, which may account for the differing rates of wound closure seen in diabetic populations.
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Registered trials
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