دورية أكاديمية

Knockout of formyl peptide receptor 1 reduces osteogenesis and bone healing.

التفاصيل البيبلوغرافية
العنوان: Knockout of formyl peptide receptor 1 reduces osteogenesis and bone healing.
المؤلفون: Yang X; Dept of Orthopaedic Surgery, University of Virginia, Charlottesville, VA, USA., Xiao W; Dept of Orthopaedic Surgery, University of Virginia, Charlottesville, VA, USA; Department of Orthopedics, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China., Le Q; Dept of Orthopaedic Surgery, University of Virginia, Charlottesville, VA, USA., Zhang Z; Dept of Orthopaedic Surgery, University of Virginia, Charlottesville, VA, USA; Dept of Orthopaedic Surgery, The First Affiliated Hospital of Xinxiang Medical University, Wehui 453100, Henan, China., Wang W; Dept of Orthopaedic Surgery, University of Virginia, Charlottesville, VA, USA., Lee SH; Dept of Mechanical & Aerospace Engineering, Center for Applied Biomechanics, University of Virginia, Charlottesville, VA, USA., Dighe A; Dept of Orthopaedic Surgery, University of Virginia, Charlottesville, VA, USA., Kerrigan JR; Dept of Mechanical & Aerospace Engineering, Center for Applied Biomechanics, University of Virginia, Charlottesville, VA, USA., Cui Q; Dept of Orthopaedic Surgery, University of Virginia, Charlottesville, VA, USA. Electronic address: qc4q@virginia.edu.
المصدر: Life sciences [Life Sci] 2024 May 01; Vol. 344, pp. 122583. Date of Electronic Publication: 2024 Mar 19.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Elsevier Country of Publication: Netherlands NLM ID: 0375521 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1879-0631 (Electronic) Linking ISSN: 00243205 NLM ISO Abbreviation: Life Sci Subsets: MEDLINE
أسماء مطبوعة: Publication: <2008->: Amsterdam : Elsevier
Original Publication: Oxford; Elmsford, N. Y. [etc.] Pergamon Press.
مواضيع طبية MeSH: Osteogenesis* , Receptors, Formyl Peptide*/genetics , Receptors, Formyl Peptide*/metabolism, Mice ; Animals ; Mice, Knockout ; Fracture Healing ; Femur/metabolism ; Cell Differentiation ; Bone Marrow Cells
مستخلص: Aims: Formyl peptide receptor 1 (FPR1), from a G-protein coupled receptor family, was previously well-characterized in immune cells. But the function of FPR1 in osteogenesis and fracture healing was rarely reported. This study, using the FPR1 knockout (KO) mouse, is one of the first studies that try to investigate FPR1 function to osteogenic differentiation of bone marrow-derived stem cells (BMSCs) in vitro and bone fracture healing in vivo.
Materials and Methods: Primary BMSCs were isolated from both FPR1 KO and wild type (WT) mice. Cloned mouse BMSCs (D1 cells) were used to examine role of FoxO1 in FPR1 regulation of osteogenesis. A closed, transverse fracture at the femoral midshaft was created to compare bone healing between KO and WT mice. Biomechanical and structural properties of femur were compared between healthy WT and KO mice.
Key Findings: FPR1 expression increased significantly during osteogenesis of both primary and cloned BMSCs. Compared to BMSCs from FPR1 KO mice, WT BMSCs displayed considerably higher levels of osteogenic markers as well as mineralization. Osteogenesis by D1 cells was inhibited by either an FPR1 antagonist cFLFLF or a specific inhibitor of FoxO1, AS1842856. In addition, the femur from WT mice had better biomechanical properties than FPR1 KO mice. Furthermore, bone healing in WT mice was remarkably improved compared to FPR1 KO mice analyzed by X-ray and micro-CT.
Significance: These findings indicated that FPR1 played a vital role in osteogenic differentiation and regenerative capacity of fractured bone, probably through the activation of FoxO1 related signaling pathways.
Competing Interests: Declaration of competing interest The authors declare that they have no competing interests.
(Copyright © 2024. Published by Elsevier Inc.)
فهرسة مساهمة: Keywords: Bone healing; Bone marrow derived stem cells; Formyl peptide receptors; Osteogenesis
المشرفين على المادة: 0 (Receptors, Formyl Peptide)
تواريخ الأحداث: Date Created: 20240320 Date Completed: 20240405 Latest Revision: 20240405
رمز التحديث: 20240405
DOI: 10.1016/j.lfs.2024.122583
PMID: 38508232
قاعدة البيانات: MEDLINE