Fracture healing involves rapid stem and progenitor cell migration, homing, and differentiation. SDF-1 (CXCL12) is considered a master regulator of CXCR4-positive stem and progenitor cell trafficking to sites of ischemic (hypoxic) injury and regulates their subsequent differentiation into mature reparative cells. In this study, we investigated the role of SDF-1/CXCR4 signaling in fracture healing where vascular disruption results in hypoxia and SDF-1 expression. Mice were injected with AMD3100, a CXCR4 antagonist, or vehicle twice daily until euthanasia with the intent to impair stem cell homing to the fracture site and/or their differentiation. Fracture healing was evaluated using micro-computed tomography, histology, quantitative PCR, and mechanical testing. AMD3100 administration resulted in a significantly reduced hyaline cartilage volume (day 14), callus volume (day 42) and mineralized bone volume (day 42) and reduced expression of genes associated with endochondral ossification including collagen Type 1 alpha 1, collagen Type 2 alpha 1, vascular endothelial growth factor, Annexin A5, nitric oxide synthase 2, and mechanistic target of rapamycin. Our data suggest that the SDF-1/CXCR4 signaling plays a central role in bone healing possibly by regulating the recruitment and/or differentiation of stem and progenitor cells.
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http://dx.doi.org/10.1002/jor.22145 | DOI Listing |
Introduction: In this study, we tested the hypothesis that pre-osteoclast signaling is key in triggering post-traumatic angiogenesis in alveolar bone via the SDF-1/CXCR4 pathway. Interruption of osteoclast differentiation through zoledronate (Zol) disrupts the crosstalk between pre-osteoclasts and endothelial cells, hindering the initial angiogenic reaction following dental trauma. This disruption could therefore play a role in the pathogenesis of medication-related osteonecrosis of the jaw (MRONJ).
View Article and Find Full Text PDFBiomed Pharmacother
December 2024
Institute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-inflammatory and Immune Medicine, Ministry of Education, Hefei 230032, China; Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Hefei 230032, China; Laboratory Animal Center, Anhui Medical University, Hefei 230032, China. Electronic address:
Background: The intrinsic healing ability of articular cartilage is poor after injury or illness, and untreated injury could lead to cartilage degeneration and ultimately osteoarthritis. iMSCs are derived from embryonic induced pluripotent stem cells and have strong therapeutic capabilities in the repair of cartilage defects, while the mechanism of action is unclear. The aim of this study is to clarify the repair mode of iMSCs on cartilage defects in rat knee joints, elucidate the chemotactic effect of iMSCs on autologous BMSCs in rats, and provide a basis for the treatment of cartilage defects and endogenous regeneration with iMSCs.
View Article and Find Full Text PDFBiomolecules
September 2024
Department of Histology and Embryology, Shantou University Medical College, No. 22 Xinling Road, Shantou 515041, China.
Chronic stress is a common cause of hair loss, involving inflammatory responses and changes in cellular signaling pathways. This study explores the mechanism of action of the SDF-1/CXCR4 signaling axis in chronic stress-induced hair loss. The research indicates that SDF-1 promotes hair follicle growth through the PI3K/Akt and JAK/STAT signaling pathways.
View Article and Find Full Text PDFCell Signal
December 2024
Huzhou Central Hospital, The Fifth School of Clinical Medicine of Zhejiang Chinese Medical University, Huzhou, China; Huzhou Key Laboratory of Basic Research and Clinical Translation for Neuromodulation, Huzhou, China. Electronic address:
Cells
August 2024
Institute of Clinical Medicine, National Yang Ming Chiao Tung University, Taipei 11221, Taiwan.
Colorectal cancer (CRC) is a leading cause of cancer mortality worldwide, and cancer-associated fibroblasts (CAFs) play a major role in the tumor microenvironment (TME), which facilitates the progression of CRC. It is critical to understand how CAFs promote the progression of CRC for the development of novel therapeutic approaches. The purpose of this study was to understand how CAF-derived stromal-derived factor-1 (SDF-1) and its interactions with the corresponding C-X-C motif chemokine receptor 4 (CXCR4) promote CRC progression.
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