SDF-1 mediates mesenchymal stem cell recruitment and migration via the SDF-1/CXCR4 axis in bone defect
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ORIGINAL ARTICLE
SDF‑1 mediates mesenchymal stem cell recruitment and migration via the SDF‑1/CXCR4 axis in bone defect Heli Zhang1 · Xijing Li2 · Junfeng Li3 · Lili Zhong4 · Xue Chen5 · Si Chen6 Received: 25 April 2019 / Accepted: 27 June 2020 © The Japanese Society Bone and Mineral Research and Springer Japan KK, part of Springer Nature 2020
Abstract Introduction Recent studies have indicated the potential of stem cell therapy in combination with cytokines to restore the bone repair via migration and homing of stem cells to the defected area. The present study aimed to investigate the mobilization and recruitment of mesenchymal stem cells (MSCs) in response to SDF-1. Materials and Methods Herein, the knockout rat model of the bone defect (BD) was treated with the induced membrane technique. Then, wild type Wistar rats and SDF-1-knockout rats were selected for the establishment of BD-induced membrane (BD-IM) models and bone-graft (BG) models. The number of MSCs was evaluated by flow cytometry, along with the expression pattern of the SDF-1/CXCR4 axis as well as osteogenic factors was identified by RT-qPCR and Western blot analyses. Finally, the MSC migration ability was assessed by the Transwell assay. Results Our data illustrated that in the induced membrane tissues, the number of MSCs among the BD-IM modeled rats was increased, whereas, a lower number was documented among BG modeled rats. Besides, we found that lentivirus-mediated over-expression of SDF-1 in BG modeled rats could activate the SDF-1/CXCR4 axis, mobilize MSCs into the defect area, and up-regulate the osteogenic proteins. Conclusions Collectively, our study speculated that up-regulation of SDF-1 promotes the mobilization and migration of MSCs through the activation of the SDF-1/CXCR4 signal pathway. Keywords Stromal cell-derived factor-1 · SDF-1/CXCR4 axis · Bone defect · Bone graft · Induced membrane technique Heli Zhang, Xijing Li have contributed equally to this work. * Xue Chen [email protected] * Si Chen [email protected] 1
Department of Outpatient, The Second Hospital of Jilin University, Changchun 130041, People’s Republic of China
2
Department of Emergency, The Second Hospital of Jilin University, Changchun 130041, People’s Republic of China
3
Department of Clinical Laboratory, The Second Hospital of Jilin University, Changchun 130041, People’s Republic of China
4
Jilin Provincial Key Laboratory On Molecular and Chemical Genetic, The Second Hospital of Jilin University, Changchun 130041, People’s Republic of China
5
Department of Orthopedics, The Second Hospital of Jilin University, No. 218, Ziqiang Street, Nanguan District, Changchun 130041, Jilin, People’s Republic of China
6
Department of Geriatric Medicine, The Second Hospital of Jilin University, No. 218, Ziqiang Street, Nanguan District, Changchun 130041, Jilin, People’s Republic of China
Introduction An array of factors have been identified as the causative reason for bone defect (BD), including tumors, infection, and trauma, among which tr
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