دورية أكاديمية
Augmented effect of fibroblast growth factor 18 in bone morphogenetic protein 2-induced calvarial bone healing by activation of CCL2/CCR2 axis on M2 macrophage polarization
| العنوان: | Augmented effect of fibroblast growth factor 18 in bone morphogenetic protein 2-induced calvarial bone healing by activation of CCL2/CCR2 axis on M2 macrophage polarization |
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| المؤلفون: | Worachat Namangkalakul, Shigenori Nagai, Chengxue Jin, Ken-ichi Nakahama, Yuki Yoshimoto, Satoshi Ueha, Kazunari Akiyoshi, Kouji Matsushima, Tomoki Nakashima, Masaki Takechi, Sachiko Iseki |
| المصدر: | Journal of Tissue Engineering, Vol 14 (2023) |
| بيانات النشر: | SAGE Publishing, 2023. |
| سنة النشر: | 2023 |
| المجموعة: | LCC:Biochemistry |
| مصطلحات موضوعية: | Biochemistry, QD415-436 |
| الوصف: | Fibroblast growth factor (FGF) signaling plays essential roles in various biological events. FGF18 is one of the ligands to be associated with osteogenesis, chondrogenesis and bone healing. The mouse critical-sized calvarial defect healing induced by the bone morphogenetic protein 2 (BMP2)-hydrogel is stabilized when FGF18 is added. Here, we aimed to investigate the role of FGF18 in the calvarial bone healing model. We first found that FGF18 + BMP2 hydrogel application to the calvarial bone defect increased the expression of anti-inflammatory markers, including those related to tissue healing M2 macrophage (M2-Mø) prior to mineralized bone formation. The depletion of macrophages with clodronate liposome hindered the FGF18 effect. We then examined how FGF18 induces M2-Mø polarization by using mouse primary bone marrow (BM) cells composed of macrophage precursors and BM stromal cells (BMSCs). In vitro studies demonstrated that FGF18 indirectly induces M2-Mø polarization by affecting BMSCs. Whole transcriptome analysis and neutralizing antibody treatment of BMSC cultured with FGF18 revealed that chemoattractant chemokine (c-c motif) ligand 2 (CCL2) is the major mediator for M2-Mø polarization. Finally, FGF18-augmented activity toward favorable bone healing with BMP2 was diminished in the calvarial defect in Ccr2- deleted mice. Altogether, we suggest a novel role of FGF18 in M2-Mø modulation via stimulation of CCL2 production in calvarial bone healing. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 2041-7314 20417314 |
| Relation: | https://doaj.org/toc/2041-7314 |
| DOI: | 10.1177/20417314231187960 |
| URL الوصول: | https://doaj.org/article/81cdec4b4dc8450da5d5cbe4e3b6cf0d |
| رقم الأكسشن: | edsdoj.81cdec4b4dc8450da5d5cbe4e3b6cf0d |
| قاعدة البيانات: | Directory of Open Access Journals |
Full Text Finder | تدمد: | 20417314 |
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| DOI: | 10.1177/20417314231187960 |