ArticleCell death & disease2018
JAM-A knockdown accelerates the proliferation and migration of human keratinocytes, and improves wound healing in rats via FAK/Erk signaling.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 47 citations in OpenAlex.
- Mechanoresponsive ion channels Piezo1 and TRPV4 stimulate ADAM10 and ADAM17 with differential impact on endothelial migration and proliferation.Cell communication and signaling : CCS · 2026Article
- Keratinocyte Capability for Smooth Sheet Formation on a Step Pattern Substrate.Bioengineering (Basel, Switzerland) · 2025Article
- Single-cell RNA sequencing identifies the prolactin receptor as a therapeutic target in adenomyosis.Signal transduction and targeted therapy · 2025Article
- Effect ofBiomedical reports · 2025Article
- Focal Adhesion Kinase and Colony Stimulating Factors: Intestinal Homeostasis and Innate Immunity Crosstalk.Cells · 2024Review
- Identifying the roles of miR-17 in ciliogenesis and cell cycle.Frontiers in cell and developmental biology · 2024Article
- The EGF/EGFR axis and its downstream signaling pathways regulate the motility and proliferation of cultured oral keratinocytes.FEBS open bio · 2023Article
- Optogenetic engineered umbilical cord MSC-derived exosomes for remodeling of the immune microenvironment in diabetic wounds and the promotion of tissue repair.Journal of nanobiotechnology · 2023Article
- Epithelial JAM-A is fundamental for intestinal wound repair in vivo.JCI insight · 2022Article
- Type 2 Inflammation Contributes to Skin Barrier Dysfunction in Atopic Dermatitis.JID innovations : skin science from molecules to population health · 2022Review
- Article
- JAM-A signals through the Hippo pathway to regulate intestinal epithelial proliferation.iScience · 2022Article
- Gut homeostasis, injury, and healing: New therapeutic targets.World journal of gastroenterology · 2022Review
- Using the Power of Junctional Adhesion Molecules Combined with the Target of CAR-T to Inhibit Cancer Proliferation, Metastasis and Eradicate Tumors.Biomedicines · 2022Article
- The Roles of Junctional Adhesion Molecules (JAMs) in Cell Migration.Frontiers in cell and developmental biology · 2022Review
- MIR21-induced loss of junctional adhesion molecule A promotes activation of oncogenic pathways, progression and metastasis in colorectal cancer.Cell death and differentiation · 2021Article
- Norcantharidin Suppresses YD-15 Cell Invasion Through Inhibition of FAK/Paxillin and F-Actin Reorganization.Molecules (Basel, Switzerland) · 2019Article
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Junctional adhesion molecule-A (JAM-A) belongs to the immunoglobulin superfamily, it predominantly exists at the tight junctions of epithelial and endothelial cells. JAM-A is known to regulate leukocyte trans-endothelial migration, however, how it affects the proliferation and migration of keratinocytes, the two essential steps during wound healing, has less been explored. In this study, we showed that JAM-A was significantly expressed in normal skin epidermis. RNAi-mediated JAM-A knockdown remarkably promoted the proliferation and migration of keratinocytes. We also found that loss of JAM-A increased the protein levels of p-FAK, p-Erk1/2, and p-JNK; however, FAK inhibitor PF-562271 restrained the expression of p-FAK and p-Erk1/2 elevated by JAM-A RNAi, but not p-JNK, and also slowed down keratinocyte proliferation and migration. Finally, in a rat wound model we showed that absence of JAM-A significantly promoted the wound healing process, while the use of PF-562271 or Erk1/2 inhibitor PD98059 repressed those effects. These data collectively demonstrate that suppressing JAM-A expression could promote the proliferation and migration of keratinocytes and accelerate the healing process of rat skin wounds, potentially via FAK/Erk pathway, indicating that JAM-A might serve as a potential therapeutic target for the treatment of chronic refractory wounds.
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