HMGB1 can activate cartilage progenitor cells in response to cartilage injury through the CXCL12/CXCR4 pathway

Introduction: Recent studies have suggested that cartilage progenitor cells (CPCs) could be activated and differentiated into chondrocytes to produce matrix and to restore the integrity of damaged cartilage after injury. However, the mechanism involved in CPC activation upon damage is still unclear. This study aims to investigate the role of high mobility group box chromosomal protein 1 (HMGB1) in both activation and migration of CPCs during cartilage injury. Material and methods: Explants harvested from mature bovine stifle joints were used for impact injury. The proliferation and migration of CPCs were examined via confocal imaging. Gene and protein expression of Hmbg1, Cxcl12, and Cxcr4 was also examined by quantitative polymerase chain reaction (qPCR), ELISA, and western blot. Each experiment was repeated 3 times. ANOVA and Student’s t-test were performed for statistical analysis. Results: HMGB1 released from dead and damaged chondrocytes after an impact injury could activate CPCs in the superficial zone of cartilage and promote their migration and proliferation to injury sites. However, the block of HMGB1 activation with its specific binding inhibitor glycyrrhizin inhibits the proliferation and migration of CPCs. Further investigations demonstrate that HMGB1 promotes CPCs migration through the pathway of C-X-C motif chemokine 12 (CXCL12) and its receptor CXCR4. Quantitative analysis of HMGB1 in cell culture medium also indicates that CPCs may have a self-activation property after the HMGB1 released from dead cells has been exhausted. Conclusion: HMGB1 is a pivotal factor that could enhance the migration and proliferation of CPCs through the CXCL12/CXCR4 pathway after cartilage injury, which could provide useful information for cartilage repair and osteoarthritis treatment

Prevalence and risk factors for perioperative complications of CKD patients undergoing elective hip surgery

Abstract Purpose Chronic kidney disease (CKD) is known to increase morbidity and mortality after orthopedic surgery. The purpose of this study is to investigate how CKD affects perioperative complications in hip surgery patients. Material and methods From 2013 to 2016, a total of 230 patients (30 patients with CKD and 200 without CKD) undergoing hip surgery were enrolled in this study. Preoperative, intraoperative, and postoperative data was collected and analyzed between CKD and non-CKD patients. Logistic regression was used to evaluate the independent risk factor for postoperative complications. Results There were significant differences in the number of people with hypertension (90.0% vs 27.3%, P < 0.001), diabetes (33.3% vs 8.7%, P = 0.01), coronary heart disease (20.0% vs 2.0%, P = 0.001), smoking habits (56.7% vs 22.7%, P = 0.016), anemia (90.0% vs 19.3%, P < 0.001), and low hemoglobin levels (94.1 ± 19.7 vs 121.3 ± 18.8, P < 0.001) between CKD and non-CKD patients before surgery. Receiving a blood transfusion was significantly more common in CKD patients (50% vs 28.5%, P = 0.018). Postoperatively, significant differences were detected in the average number of patients who transferred to the ICU (73.3% vs 19.3%, P < 0.001). Furthermore, differences were found in the quantity of hemoglobin (92.5 ± 16.8 vs 107.5 ± 18.3, P < 0.001) and albumin (32.4 ± 4.1 vs 34.9 ± 5.5, P = 0.02) measured between CKD and non-CKD patients. Logistic regression analysis indicated that diabetes, alcohol, and anemia were all independent risk factors for obtaining a blood transfusion, while age, CKD, and osteoporosis were all independent risk factors for ICU transfers. Conclusion Compared with non-CKD patients, CKD patients were accompanied with more cardiac diseases preoperatively. In addition, CKD patients were more likely to receive a blood transfusion and transfer to the ICU after hip surgery. Preoperative anemia should be restored sufficiently to decrease the incidence of blood transfusions

Spirometra mansoni sparganosis identified by metagenomic next-generation sequencing: a case report

A 30-year-old male patient had a cyst on the left hip and progressive enlargement for more than 2 months. Combined blood tests, magnetic resonance imaging, and pathology findings, cysticercosis infection was suspected. However, the treatment for cysticercosis was ineffective. We conducted a metagenomic next-generation sequencing (mNGS) analysis on the formalin-fixed, paraffin-embedded specimen of the patient's surgically excised tissue, and the results suggested Spirometra mansoni, mNGS was further confirmed by polymerase chain reaction and phylogenetic analysis of cytochrome c oxidase subunit 1 (cox1) gene. Based on these results, we found that mNGS provided a better method of diagnosing parasitic infections

Bioprinted constructs that simulate nerve–bone crosstalk to improve microenvironment for bone repair

Crosstalk between nerves and bone is essential for bone repair, for which Schwann cells (SCs) are crucial in the regulation of the microenvironment. Considering that exosomes are critical paracrine mediators for intercellular communication that exert important effects in tissue repair, the aim of this study is to confirm the function and molecular mechanisms of Schwann cell-derived exosomes (SC-exos) on bone regeneration and to propose engineered constructs that simulate SC-mediated nerve–bone crosstalk. SCs promoted the proliferation and differentiation of bone marrow mesenchymal stem cells (BMSCs) through exosomes. Subsequent molecular mechanism studies demonstrated that SC-exos promoted BMSC osteogenesis by regulating the TGF-β signaling pathway via let-7c-5p. Interestingly, SC-exos promoted the migration and tube formation performance of endothelial progenitor cells. Furthermore, the SC-exos@G/S constructs were developed by bioprinting technology that simulated SC-mediated nerve–bone crosstalk and improved the bone regeneration microenvironment by releasing SC-exos, exerting the regulatory effect of SCs in the microenvironment to promote innervation, vascularization, and osteogenesis and thus effectively improving bone repair in a cranial defect model. This study demonstrates the important role and underlying mechanism of SCs in regulating bone regeneration through SC-exos and provides a new engineered strategy for bone repair