ArticlePloS one2017
Hypoxia Regulates mTORC1-Mediated Keratinocyte Motility and Migration via the AMPK Pathway.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
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- Dual Nanostructured Lipid Carriers/Hydrogel System for Delivery of Curcumin for Topical Skin Applications.Biomolecules · 2022Article
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- The regulation of skin homeostasis, repair and the pathogenesis of skin diseases by spatiotemporal activation of epidermal mTOR signaling.Frontiers in cell and developmental biology · 2022Review
- mTOR Signaling as a Regulator of Hematopoietic Stem Cell Fate.Stem cell reviews and reports · 2021Review
- Unlocking mammalian regeneration through hypoxia inducible factor one alpha signaling.Biomaterials · 2021Review
- The mTORC1/eIF4E/HIF-1α Pathway Mediates Glycolysis to Support Brain Hypoxia Resistance in the Gansu Zokor,Frontiers in physiology · 2021Article
- Medium conditioned by human mesenchymal stromal cells reverses low serum and hypoxia-induced inhibition of wound closure.Biochemical and biophysical research communications · 2020Article
- Electric field down-regulates CD9 to promote keratinocytes migration through AMPK pathway.International journal of medical sciences · 2020Article
- Contribution of Rho-kinase and Adenosine Monophosphate-Activated Protein Kinase Signaling Pathways to Endothelium-Derived Contracting Factors Responses.Turkish journal of pharmaceutical sciences · 2017Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Keratinocyte migration, the initial event and rate-limiting step in wound healing, plays a vital role in restoration of the intact skin barrier, also known as re-epithelialization. After acute tissue injury, hypoxic microenvironment gradually develops and acts as an early stimulus to initiate the healing process. Although we have previously found that hypoxia induces keratinocyte migration, the underlying mechanism remains unknown. Here, we first observed that hypoxia increased mTORC1 activity. Recombinant lentivirus vector and Rapamycin were used for silencing mTORC1 in HaCaT cells and primary mouse keratinocytes (MKs). Using cell migration assay and a Zeiss chamber equipped with imaging system, we also demonstrated that mTORC1 downregulation reversed hypoxia-induced keratinocyte motility and lateral migration. Importantly, hypoxia-activated mTORC1 was accompanied by the AMPK downregulation, and we found that the AMPK pathway activators Metformin (Met) and 5-Aminoimidazole-4-carboxamide 1-β-D-ribofuranoside (AICAR) decreased the mTORC1 activity, cell motility and lateral migration. Thus, our results suggest that hypoxia regulates mTORC1-mediated keratinocyte motility and migration via the AMPK pathway.
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