ArticleThe Journal of investigative dermatology2017
Ganglioside GM3 Mediates Glucose-Induced Suppression of IGF-1 Receptor-Rac1 Activation to Inhibit Keratinocyte Motility.
Article in The Journal of investigative dermatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- The efficacy of platelet-derived extracellular vesicles in the treatment of diabetic wounds: a systematic review and meta-analysis of animal studies.Archives of dermatological research · 2025Pooled it
- Lipidomic perspectives on the role of lactosylceramides in inflammation and disease: A narrative review.Expert reviews in molecular medicine · 2026Review
- Ganglioside GM3 in the Tumor Microenvironment: Mechanisms of Signaling Regulation and Strategies for Angiogenesis Inhibition.Biomolecules · 2026Review
- Unlocking the therapeutic potential of sphingolipids in wound healing: from molecular mechanisms to clinical applications.International journal of surgery (London, England) · 2026Review
- Anthrax ET activates Rac1 and RTK signaling to induce F-actin reorganization and endothelial permeability.iScience · 2025Article
- From inflammation to healing: the crucial role of GPR91 activation and SDH inhibition in chronic diabetic wound recovery.Stem cell research & therapy · 2025Article
- HEXA-FC protein therapy increases skeletal muscle glucose uptake and improves glycaemic control in mice with insulin resistance and in a mouse model of type 2 diabetes.Diabetologia · 2025Article
- Article
- Keratinocyte-Derived Exosomes in Painful Diabetic Neuropathy.bioRxiv : the preprint server for biology · 2024Article
- The Human Ganglioside Interactome in Live Cells Revealed Using Clickable Photoaffinity Ganglioside Probes.Journal of the American Chemical Society · 2024Article
- Klotho inhibits renal ox-LDL deposition via IGF-1R/RAC1/OLR1 signaling to ameliorate podocyte injury in diabetic kidney disease.Cardiovascular diabetology · 2023Article
- Gangliosides in nervous system development, regeneration, and pathologies.Neural regeneration research · 2023Review
- The contribution of intestinal Streptococcus to the pathogenesis of diabetic foot ulcers: An analysis based on 16S rRNA sequencing.International wound journal · 2022Article
- Epigenetics: key to improve delayed wound healing in type 2 diabetes.Molecular and cellular biochemistry · 2022Review
- Cutaneous innervation in impaired diabetic wound healing.Translational research : the journal of laboratory and clinical medicine · 2021Review
- Multiplicity of Glycosphingolipid-Enriched Microdomain-Driven Immune Signaling.International journal of molecular sciences · 2021Review
- Epidermal SR-A Complexes Are Lipid Raft Based and Promote Nucleic Acid Nanoparticle Uptake.The Journal of investigative dermatology · 2021Article
- A Comprehensive Review: Sphingolipid Metabolism and Implications of Disruption in Sphingolipid Homeostasis.International journal of molecular sciences · 2021Review
- Essential Functions of Glycans in Human Epithelia Dissected by a CRISPR-Cas9-Engineered Human Organotypic Skin Model.Developmental cell · 2020Article
- Flotillin and AP2A1/2 Promote IGF-1 Receptor Association with Clathrin and Internalization in Primary Human Keratinocytes.The Journal of investigative dermatology · 2020Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Activation of insulin-like growth factor-1 (IGF-1) receptor (IGF1R) signaling induces keratinocyte migration, but little is known about its regulation, including in diabetic wounds. GM3, a lipid raft ganglioside synthesized by GM3 synthase (GM3S), regulates receptor signaling. In diabetic mice, knockout or topically applied nanoconstruct-mediated knockdown of GM3S promotes wound edge IGF1R phosphorylation and re-epithelialization. Through modulating GM3 expression, we explored the role of GM3 in regulating human keratinocyte IGF1R signaling. Increases in GM3 and GM3S expression, including by exposure to high glucose, inhibit keratinocyte migration and IGF-1-induced chemotaxis in association with inhibition of IGF1R phosphorylation, suppression of Rac1 signaling, and activation of RhoA signaling. In contrast, GM3 depletion accelerates cell migration; increases cell velocity, displacement, and persistence; and activates IGF1R-Rac1 signaling. These data implicate GM3 in mediating glucose-induced suppression of IGF1R-Rac1 signaling. Furthermore, our findings provide evidence of a pivotal role for GM3-induced insulin resistance in impairing keratinocyte migration and reinforce the previously published studies in diabetic mice supporting GM3-depleting strategies as an approach for accelerating the healing of human diabetic wounds.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.