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Are hypoxia-related proteins associated with the invasiveness of glandular odontogenic cysts? A multicenter study.
Arch Oral Biol
November 2024
Laboratory of Histopathology and Immunohistochemistry, School of Dentistry, Universidade Federal do Pará, Belém, Pará, Brazil. Electronic address:
Objective: The study aimed to investigate the expression of hypoxia markers associated with invadopodia in glandular odontogenic cysts and to explore an association between this expression with the aggressive biological behaviour of this odontogenic cyst.
Design: Immunohistochemistry was employed to assess the expression of hypoxia-inducible factor 1 alpha (HIF-1α), notch homologous protein of the neurogenic locus 1 (NOTCH-1), disintegrin and metalloproteinase-12 (ADAM-12), and heparin-binding epidermal growth factor (HB-EGF) in 17 samples of glandular odontogenic cysts, 10 samples of calcifying odontogenic cysts, and 10 samples of dental follicles.
Results: The glandular odontogenic cyst samples exhibited increased expression of HIF-1α, NOTCH-1, ADAM-12 and HBEGF proteins compared with calcifying odontogenic cyst and dental follicle samples.
Low-affinity ligands of the epidermal growth factor receptor are long-range signal transmitters in collective cell migration of epithelial cells.
Cell Rep
November 2024
Department of Pathology and Biology of Diseases, Graduate School of Medicine, Kyoto University, Yoshida-Konoe-Cho, Sakyo-ku, Kyoto 606-8501, Japan; Graduate School of Medicine, Tokushima University, Shinkura-cho, Tokushima 770-8501, Japan. Electronic address:
Article Synopsis
- The study explores how low-affinity EGFR ligands, specifically epiregulin (EREG), activate the EGFR in cells during processes like collective cell migration.
- It reveals that during this migration, certain patterns of signal activation occur that depend on the shedding of EGFR ligands and the structural integrity of cell junctions.
- The absence of EREG in mice leads to slower ERK wave propagation and less effective cell movement, suggesting that low-affinity ligands are crucial for quick signaling between cells.
The generation of stable microvessels in ischemia is mediated by endothelial cell derived TRAIL.
Sci Adv
October 2024
Heart Research Institute, The University of Sydney, Sydney, Australia.
Reversal of ischemia is mediated by neo-angiogenesis requiring endothelial cell (EC) and pericyte interactions to form stable microvascular networks. We describe an unrecognized role for tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in potentiating neo-angiogenesis and vessel stabilization. We show that the endothelium is a major source of TRAIL in the healthy circulation compromised in peripheral artery disease (PAD).
View Article and Find Full Text PDFLactate-Induced HBEGF Shedding and EGFR Activation: Paving the Way to a New Anticancer Therapeutic Opportunity.
Cells
September 2024
Department of Medical and Surgical Sciences (DIMEC), Section of General Pathology, University of Bologna, 40126 Bologna, Italy.
Cancer cells can release EGF-like peptides, acquiring the capacity of autocrine stimulation via EGFR-mediated signaling. One of these peptides (HBEGF) was found to be released from a membrane-bound precursor protein and is critically implicated in the proliferative potential of cancer cells. We observed that the increased lactate levels characterizing neoplastic tissues can induce the release of uPA, a protease promoting HBEGF shedding.
View Article and Find Full Text PDFStaphylococcus epidermidis augments human β-defensin-3 synthesis through the transforming growth factor alpha-epidermal growth factor receptor cascade.
J Dermatol Sci
October 2024
Department of Dermatology, Nara Medical University, Kashihara, Japan.
Background: Epidermal growth factor receptor inhibitors (EGFRIs) reduce β-defensin 3 (BD3) from keratinocytes stimulated by S. epidermidis, potentially leading to the development of acneiform rashes in patients undergoing EGFRIs treatment. However, the mechanism through which S.
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