1.Application of vacuum sealing drainage in the treatment of severe maxillofacial and neck space infection
Dongyuan QI ; Rui ZHANG ; Yuanlong ZHAO ; Ru WANG
Journal of Practical Stomatology 2017;33(6):824-826
Objective:To investigate the efficacy of vacuum sealing drainage (VSD) in the treatment of severe maxillofacial and neck space infection.Methods:9 patients (6 males,3 females) with severe maxillofacial and neck space infection were treated with VSD.After incision of abscess,the incision was covered by VSD material and 40-60 KPa continuous negative pressure drainage was given.Results:Swelling and pain of the patients reduced rapidly.The period of VSD treatment was 4 to 10 days (mean 5.8 days).9 patients were all cured without mediastinitis.Conclusion:VSD ehhance the dranage efficiency and prevent infection spreading.
2.Carcinoma-associated fibroblast-derived lysyl oxidase-rich extracellular vesicles mediate collagen crosslinking and promote epithelial-mesenchymal transition via p-FAK/p-paxillin/YAP signaling.
Xue LIU ; Jiao LI ; Xuesong YANG ; Xiaojie LI ; Jing KONG ; Dongyuan QI ; Fuyin ZHANG ; Bo SUN ; Yuehua LIU ; Tingjiao LIU
International Journal of Oral Science 2023;15(1):32-32
Carcinoma-associated fibroblasts (CAFs) are the main cellular components of the tumor microenvironment and promote cancer progression by modifying the extracellular matrix (ECM). The tumor-associated ECM is characterized by collagen crosslinking catalyzed by lysyl oxidase (LOX). Small extracellular vesicles (sEVs) mediate cell-cell communication. However, the interactions between sEVs and the ECM remain unclear. Here, we demonstrated that sEVs released from oral squamous cell carcinoma (OSCC)-derived CAFs induce collagen crosslinking, thereby promoting epithelial-mesenchymal transition (EMT). CAF sEVs preferably bound to the ECM rather than being taken up by fibroblasts and induced collagen crosslinking, and a LOX inhibitor or blocking antibody suppressed this effect. Active LOX (αLOX), but not the LOX precursor, was enriched in CAF sEVs and interacted with periostin, fibronectin, and bone morphogenetic protein-1 on the surface of sEVs. CAF sEV-associated integrin α2β1 mediated the binding of CAF sEVs to collagen I, and blocking integrin α2β1 inhibited collagen crosslinking by interfering with CAF sEV binding to collagen I. CAF sEV-induced collagen crosslinking promoted the EMT of OSCC through FAK/paxillin/YAP pathway. Taken together, these findings reveal a novel role of CAF sEVs in tumor ECM remodeling, suggesting a critical mechanism for CAF-induced EMT of cancer cells.
Humans
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Paxillin/metabolism*
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Protein-Lysine 6-Oxidase/metabolism*
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Carcinoma, Squamous Cell/pathology*
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Epithelial-Mesenchymal Transition
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Integrin alpha2beta1/metabolism*
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Mouth Neoplasms/pathology*
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Collagen/metabolism*
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Fibroblasts
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Extracellular Vesicles/metabolism*
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Cell Line, Tumor
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Tumor Microenvironment