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08 January 2023, Volume 27 Issue 在线 Previous Issue    Next Issue

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Mechanical stimulation enhances matrix formation of three-dimensional bioprinted cartilage constructs Sun Kexin, Zeng Jinshi, Li Jia, Jiang Haiyue, Liu Xia 2023, 27 (在线):  1-7.  Abstract ( 490 )   PDF (2169KB) ( 100 )   Save BACKGROUND: Uneven secretion of matrix and insufficient mechanical strength are important factors affecting the formation effect of tissue engineering constructs in vivo. Mechanical stimulation is an effective means to promote the secretion of extracellular matrix. OBJECTIVE: To explore the biological performance of 3D bioprinted cartilage constructs under mechanical stimulation. METHODS: The chondrocyte-GelMA bioink was prepared and printed by 3D bioprinting technology, and the general observation, the live/dead cell staining, and the cell survival rate at each time point were analyzed; The constructs under compressing stimulation were taken as the experimental group and the constructs without stimulation were taken as the control group. After 2w culture in vitro, the cartilage formation of the two group constructs was observed by histological staining and the relative expression levels of cartilage-related genes was detected by real-time quantitative PCR. The constructs were implanted into nude mice for 5 weeks after 2w culture in vitro with or without mechanical stimulation, and the cartilage formation was observed by gross view and HE staining. RESULTS AND CONCLUSION:(1) General observation showed stable morphology and clear structure of the chondrocyte-GelMA constructs. The survival rate of cells at 1, 4, and 7 days of culture was above 90%, and the survial rate of cells in 4 and 7d was significantly higher than that in 1d. (2)The qRT-PCR results showed that the chondrogenesis-related genes ELN, COL, A1, COL IIA1, LOX were up-regulated after compressing culture for 2 weaks, and the expressions of COL IIA1 and ELN were significantly up-regulated (P < 0.05). Histology and immunohistochemical staining showed that the cartilage matrix and type I collagen deposition were more obvious in the experimental group than in the control group. (3) The in vivo results showed no obvious difference in appearance between the two groups, and the HE staining results showed that the cartilage formation were more homogeneous in the experimental group. (4) The 3D bioprinted chondrocyte-GelMA construct can maintain a stable three-dimensional structure, has a high cell survival rate, and can form cartilage tissue in vitro and in vivo. Compression stimulation may induce cell death, however, it increases the expression of cartilage specific genes of the survival cells and promotes cartilage formation.  Figures and Tables | References | Related Articles | Metrics

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Effects of sodium arsenite on human umbilical vein endothelial cell injury and sphingosine kinases 1/sphingosine 1-phosphate signaling axis Fang Xingyan, Tian Zhenli, Zhao Zheyi, Wen Ping, Xie Tingting 2023, 27 (在线):  1-7.  Abstract ( 158 )   PDF (1817KB) ( 102 )   Save BACKGROUND: Vascular endothelial cells are the main target of arsenic toxicity and the molecular mechanism of arsenic-induced endothelial cell injury needs to be further studied. OBJECTIVE: To study the effects of sodium arsenite on human umbilical vein endothelial cell injury and sphingosine kinase 1/sphingosine 1-phosphate signaling axis of human umbilical vein endothelial cells. METHODS: Human umbilical vein endothelial cells were isolated, cultured, and identified. The cells were treated with 0, 5, 10, 15, 20, 25 µmol/L sodium arsenite for 24 hours. Cell viability was detected by cell counting kit-8. Cell morphology was observed by inverted phase contrast microscope. The content of intracellular reactive oxygen species was detected by fluorescent probe DCFH-DA. Annexin V-FITC/PI double labeling combined with flow cytometry and TUNEL were used to detect apoptosis. The content of sphingosine 1-phosphate in cells was detected by ELISA. The mRNA and protein expressions of vascular cell adhesion molecule-1, sphingosine kinase 1, and sphingosine 1-phosphate were detected by real-time fluorescence quantitative PCR and western blot respectively.  RESULTS AND CONCLUSION: Compared with the control group (0 µmol/L sodium arsenite), the cell viability decreased gradually along with the increased concentration of sodium arsenite in a dose-dependent manner; the cell fusion rate decreased gradually, the cell gap widened gradually, and the number of exfoliated and floating cells increased gradually; the reactive oxygen species content and apoptosis rate increased gradually; the sphingosine 1-phosphate content in cells increased gradually; the relative mRNA and protein expressions of vascular cell adhesion molecule-1 and sphingosine kinase 1 increased gradually, while the relative mRNA and protein expression of sphingosine kinase 1 decreased gradually. To conclude, sodium arsenite-injured human umbilical vein endothelial cell injury may be related to the activation of sphingosine kinase 1/sphingosine 1-phosphate signaling axis and the downregulation of sphingosine 1-phosphate receptor 1. Sphingosine kinase 1/sphingosine 1-phosphate signaling axis may become a new target of arsenic-induced cardiovascular injury. Figures and Tables | References | Related Articles | Metrics

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Bone cement augmented proximal femoral nail antirotation for type A3.3 intertrochanteric femoral fracturalysis Nong Fuxiang, Jiang Zhixiong, Li Yinghao, Xu Wencong, Shi Zhilan, Luo Hui, Zhang Qinglang, Zhong Shuang, Tang Meiwen 2023, 27 (在线):  1-10.  doi: 10.12307/2023.608 Abstract ( 626 )   PDF (2265KB) ( 325 )   Save BACKGROUND: At present, studies have been done to reveal the relationship between exosomes and ferroptosis, but the research is still limited. Therefore, further exploration of the relationship between exosomes and ferroptosis will help to seek new treatment strategies and reliable basis for clinical treatment of diseases.   OBJECTIVE: To expound the biological characteristics of exosomes, the mechanism of ferroptosis, and the main ways of exosomes regulating ferroptosis, and summarize the application progress of exosomes inducing or inhibiting ferroptosis in the fields of tumor, cardiovascular system, nervous system disease and liver disease. METHODS:  Relevant articles were retrieved in CNKI and PubMed using computer. Search terms included “Exosomes, Ferroptosis, disease” in Chinese and English. Finally, 66 articles related to the research purpose of the article were included for further review.  RESULTS AND CONCLUSION: (1) Exosomes play a regulatory role in promoting cell ferroptosis by participating in iron metabolism, lipid metabolism and amino acid metabolism. (2) Exosomes play an important role in the treatment of various diseases by inducing or inhibiting ferroptosis: on the one hand, exosomes induce ferroptosis of cancer cells, inhibit tumor growth and metastasis, and improve the effect of tumor targeted therapy. On the other hand, by inhibiting ferroptosis, exosomes promote the regeneration and repair of myocardial ischemia-reperfusion and reduce cardiac toxicity in cardiovascular disease. In terms of nervous system diseases, it has played a role in inhibiting cerebral hemorrhage and reducing sepsis. In liver diseases, it can improve hepatic ischemia-reperfusion. (3) Although the specific mechanism by which exosomes regulate ferroptosis in various diseases has not been fully explored, and the relevant research is still in the preliminary stage. However, the regulation of ferroptosis by exosomes is expected to become one of the new potential targets for clinical treatment of various diseases in the future. Figures and Tables | References | Related Articles | Metrics

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Erastin inhibits proliferation of hypertrophic scar fibroblasts He Xi, Wan Yu, Tang Yuting, Yang Anning, Wu Kai, Jiao Yun, Bai Zhigang, Jiang Yideng, Shen Jiangyong 2023, 27 (在线):  1.  Abstract ( 220 )   PDF (1373KB) ( 1746 )   Save BACKGROUND: Hypertrophic scar is a kind of pathological scar that appears in the healing process after skin trauma caused by various reasons. Because there is no effective treatment, more effective treatment methods need to be sought. Objective: To investigate the effect of ferroptosis inducer (Erastin) on the proliferation of human hypertrophic scar fibroblasts. Methods: The hypertrophic scars provided by the Burn Plastic Surgery Department of the General Hospital of Ningxia Medical University and the normal skin of the same individual were collected, and human hypertrophic scar fibroblasts were extracted for subsequent experiments; The cells were divided into control group (without treatment) and ferroptosis inducer group (treated with 20 μmol/L Erastin for 24 hours) , The expression of Ferritin was detected by Western blot. iron ion detection kit to measure cellular iron ion content; malondialdehyde (MDA) detection kit to detect cellular MDA content; The cells were divided into control group (without treatment) , ferroptosis inducer group (treated with 20 μmol/L Erastin for 24 hours) and ferroptosis inducer + ferroptosis inhibitor group (treated with 20 μmol/L Erastin and 20 μmol/L Ferrostatin-1 for 24 hours) , qRT-PCR was used to detect the mRNA expression of proliferating cell nuclear antigen (PCNA) and cyclin-dependent kinase inhibitor (p27); Western blot was used to detect the protein expression of PCNA and p27; CCK8 and EdU were used to detect cell proliferation Vitality and proliferation levels. Results And Conclusion: (1) Compared with the control group, the ferritin decreased (P < 0.01), the iron ions increased (P < 0.05), the MDA increased (P < 0.01). (2) Compared with the control group, the expression of PCNA decreased (mRNA: P < 0.01, protein: P < 0.01), the expression of p27 increased (mRNA: P <  0.05, protein: P < 0.05), and the cell proliferation ability was weakened (P < 0.01), the number of EdU positive cells decreased (P < 0.01); (3) Compared with the ferroptosis inducer group, the expression of PCNA in the ferroptosis inducer + ferroptosis inhibitor group increased (mRNA: P<0.01, protein: P < 0.05), decreased p27 expression (mRNA: P < 0.01, protein: P < 0.05), enhanced cell proliferation (P < 0.01), and increased EdU-positive cells (P < 0.05). To conclude, the ferroptosis inducer (Erastin) induces ferroptosis in hypertrophic scar fibroblasts and then inhibits their proliferation, which provides a theoretical basis for finding a more effective clinical treatment method for hypertrophic scar. Figures and Tables | References | Related Articles | Metrics

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Screening and validation of neurogenic bladder miRNA-mRNA regulatory network Guo Shuhui, Yang Ye, Jiang Yangyang, Xu Jianwen 2023, 27 (在线):  1-8.  Abstract ( 139 )   PDF (2379KB) ( 194 )   Save Abstract BACKGROUND: The miRNA-mRNA regulatory network plays an important role in various biological processes, but its specific mechanism in neurogenic bladder after spinal cord injury remains unclear. OBJECTIVE: To mine the related targets of neurogenic bladder based on bioinformatics and to construct the miRNA-mRNA regulatory network, verified by animal experiments. METHODS: The differential genes of neurogenic bladder were screened from GEO database to construct the miRNA-mRNA regulatory network. The differential genes were analyzed by gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses using the David database. Protein-protein interaction analysis was performed using the STRING database. Key genes were identified by Cytoscape and ROC curves. Finally the key genes were validated by RT-PCR in a rat model of neurogenic bladder. RESULTS AND CONCLUSION: A total of 188 differential genes related to neurogenic bladder were identified. Gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses revealed that they were enriched mainly in inflammatory response, cytokine-cytokine receptor interaction, and chemokine signaling pathway. Two key regulatory networks, miR-147-brain-derived neurotrophic factor and miR-362-5p-Scn9a, were identified based on the Cytoscape and ROC curve results. RT-PCR results showed that miR-147, miR-362-5p, and brain-derived neurotrophic factor were highly expressed in the neurogenic bladder rats, while Scn9a was lowly expressed compared with the control rats. Overall, these findings indicate that miR-147-brain-derived neurotrophic factor and miR-362-5p-Scn9a actas important regulators of pathophysiological processes such as inflammation and oxidative stress, which are expected to become new targets for the diagnosis and treatment of neurogenic bladder.  Figures and Tables | References | Related Articles | Metrics

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Changes in Lumbosacral Sagittal Plane Parameters of L5/S1 Disc Herniation 2023, 27 (在线):  1-6.  Abstract ( 128 )   PDF (2011KB) ( 982 )   Save BACKGROUND: Previous studies have shown the correlation between lumbosacral sagittal plane parameters and natural absorption of lumbar disc herniation. However, the lumbosacral sagittal plane parameters included lumbar lordosis Angle, lumbosacral joint Angle, sacral inclination Angle and many other parameters, and the effects of each parameter on the natural absorption of herniated disc were different. In addition, there are few studies on reabsorption of a specific segment of intervertebral disc herniation at present, and most of the measured data are obtained from DR Or CT, while the correlation between lumbosacral sagittal plane parameters measured from MRI and reabsorption after L5/S1 intervertebral disc herniation is rarely reported.  OBJECTIVE: To study the corresponding changes of lumbar sagittal plane parameters after L5/S1 intervertebral disc herniation reabsorption and to screen out the lumbosacral sagittal plane parameters with the most significant changes during intervertebral disc reabsorption. METHODS: In this study, 57 patients with lumbar disc herniation who had complete MRI image data from February 2011 to June 2019 were selected and met the diagnostic criteria for lumbar disc herniation and only received non-surgical treatment for reabsorption of L5/S1 protrusion segments. MRI measured the protrusion area of the maximum protrusion plane in the coronal plane, lumbosacral sagittal plane parameters [lumbar curvature index (LCI), lumbar Cobb Angle (α), L5/S1 disc Angle (β), intervertebral height measurement (D), lumbosacral joint Angle (LSA), sacral platform Angle (STA), sacral inclination Angle (SS), and lower lumbar lordosis Angle (Lowe LL))]. Besides, lumbosacral sagittal plane parameters were ranked in importance of variables by random forest model in R software, and then significant variables were fitted with multiple linear regression, and the changes between parameters before and after treatment were analyzed and compared by paired sample T test.  RESULTS AND CONCLUSION: A total of 57 patients with L5/S1 lumbar disc herniation were included in this study, and the symptoms and imaging features of the patients were significantly relieved to a large extent. Before treatment, there were 4 cases of grade 1, 29 cases of grade 2 and 24 cases of grade 3. After treatment, there were 48 cases of grade 1 and 9 cases of grade 2. The random forest model suggested that intervertebral height, lumbar curve index, sacral inclination Angle, and lower lumbar lordosis Angle changed significantly in L5/S1 disc herniation reabsorption, and the order of their change significance was lumbar curve index > intervertebral space height > sacral inclination Angle > lower lumbar lordosis Angle. Lumbar curve index, lumbar Cobb Angle and sacral platform Angle increased, with statistical significance (P<0.05). There were no significant differences in disc Angle, intervertebral height, lower lumbar lordosis Angle, sacral inclination Angle and lumbosacral joint Angle (P>0.05). Lumbar curvature index was the most significant parameter of lumbosacral sagittal plane in herniated disc reabsorption. In addition, lumbar curve index, sacral inclination Angle, and lower lumbar lordosis Angle are commonly used clinically to describe the change of lumbar curvature, suggesting that L5/S1 disc herniation reabsorption is correlated with the change of lumbar curvature. Figures and Tables | References | Related Articles | Metrics

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Strategies and advance on stem cell transplantation for repair of spinal cord injury He Wanyu, Cheng Leping 2023, 27 (在线):  1-7.  Abstract ( 113 )   PDF (1985KB) ( 412 )   Save BACKGROUND: Spinal cord injury is often caused by car accidents and falls, which not only cause serious physical and psychological injuries to patients but also bring a heavy economic burden to society. Spinal cord injury is initially triggered by mechanical trauma, followed by secondary injuries, and as the disease progresses, a glial scar develops.   OBJECTIVE: To summarize the pathological process of spinal cord injury and strategies for stem cell transplantation to repair spinal cord injury, aiming to provide the best protocol for treating spinal cord injury.   METHODS: Computer search was used to search PubMed and CNKI databases. Chinese search terms were “stem cell transplantation, spinal cord injury”. English search terms were “stem cell, spinal cord injury, spinal cord, mesenchymal stem cells, neural stem cells, pathophysiology, clinical trial, primary injury, secondary injury”. The literature was screened according to the inclusion and exclusion criteria. Finally, 91 articles were included for review analysis.  RESULTS AND CONCLUSION: (1) The strategies for repairing spinal cord injury through stem cell transplantation can be divided into exogenous stem cell transplantation and endogenous stem cell transplantation. The exogenous stem cell transplantation strategy for the treatment of spinal cord injury is divided into four kinds: injecting stem cells into the site of injury; transplantation of biomaterials loaded with stem cells; fetal tissue transplantation; transplantation of engineered neural network tissue or spinal cord-like tissue. (2) Compared with a single treatment method, combination therapy can more effectively promote nerve regeneration and spinal cord function recovery. (3) Microenvironment regulating the injury site, magnetic stimulation, electrical stimulation, epidural oscillating electric field stimulation, transcription factor-mediated neural stem cell differentiation and rehabilitation therapy can be combined with stem cell transplantation for combination therapy, thereby promoting the recovery of spinal cord function. Figures and Tables | References | Related Articles | Metrics

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Knockdown of circRNA WD repeat containing protein 1 inhibits proliferation and induces apoptosis of chondrocytes in knee osteoarthritis Shen Feiyan, Yao Jixiang, Su Shanshan, Zhao Zhongmin, Tang Weidong 2023, 27 (在线):  1-6.  Abstract ( 56 )   PDF (1618KB) ( 73 )   Save BACKGROUND: Circular RNAs (circRNAs) play important roles in a variety of diseases or tumors, and recent findings have revealed that circRNAs are abnormally expressed in knee osteoarthritis and are involved in disease progression through microRNA/mRNA regulation. OBJECTIVE: To investigate the effect of circRNA WD repeat containing protein 1 (circ-BRWD1)/miR-488-3p/DNA methyltransferase 3A (DNMT3A) on the proliferation and apoptosis of chondrocytes in knee osteoarthritis. METHODS: Real-time fluorescence quantitative PCR was performed to detect the expression of circ-BRWD1, miR-488-3p, DNMT3A in knee osteoarthritis chondrocytes. Cells were divided into si-NC group, si-circ-BRWD1 group, vector group, circ-BRWD1 group, si-circ-BRWD1+anti-miR-NC group, si-circ-BRWD1+anti-miR-488-3p group, miR-NC group, miR-488-3p group, anti-miR-NC group, anti-miR-488-3p group, miR-488-3p+vector group, miR 488-3p+DNMT3A group. Real-time fluorescence quantitative PCR was used to detect circ-BRWD1, miR-488-3p, DNMT3A expression, MTT and flow cytometry assay were used to detect cell proliferation and apoptosis. Western blot assay was used to detect DNMT3A and proliferation/apoptosis-related protein expression. Dual luciferase reporter assay was used to Dual luciferase reporter assay to detect the targeting relationship of circ-BRWD1 with miR-488-3p and miR-488-3p with DNMT3A. RESULTS AND CONCLUSION: circ-BRWD1 and DNMT3A were highly expressed and miR-488-3p was lowly expressed in knee osteoarthritis chondrocytes compared with normal chondrocytes. Knockdown of circ-BRWD1 or overexpression of miR-488-3p inhibited proliferation and induced apoptosis in knee osteoarthritis chondrocytes. circ-BRWD1 targeted negative regulation of miR-488-3p and inhibition of miR-488-3p reversed the effect of circ-BRWD1 knockdown on chondrocyte proliferation and apoptosis in knee osteoarthritis. miR-488-3p targeted negative regulation of DNMT3A and upregulation of DNMT3A reversed the effect of miR-488-3p overexpression on chondrocyte proliferation and apoptosis in knee osteoarthritis. circ-BRWD1 could regulate the expression of DNMT3A by regulating miR-488-3p. To conclude, knockdown of circ-BRWD1 inhibits chondrocyte proliferation and induces apoptosis in knee osteoarthritis, and the mechanism of action may be related to the regulation of miR-488-3p/DNMT3A axis. Figures and Tables | References | Related Articles | Metrics