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  • Wang, Bingjin  (18)
  • 1
    Online Resource
    Online Resource
    Distal adding-on after surgery in Lenke 5C adolescent idiopathic scoliosis: clinical and radiological outcomes
    Springer Science and Business Media LLC ; 2022
    In:  BMC Musculoskeletal Disorders Vol. 23, No. 1 ( 2022-12)
    Details
    In: BMC Musculoskeletal Disorders, Springer Science and Business Media LLC, Vol. 23, No. 1 ( 2022-12)
    Abstract: To evaluate the incidence and risk factors of postoperative distal adding-on in patients with Lenke 5C adolescent idiopathic scoliosis (AIS). More accurate selection criteria for the lower instrumented vertebra (LIV) should be confirmed to prevent distal adding-on. Methods Forty-six patients with Lenke 5C AIS who underwent posterior fusion were enrolled in the study. Patients were allocated into adding-on and no adding-on groups. Demographic data, clinical data, and radiographic parameters were recorded and compared. Results Postoperative distal adding-on occurred in eight patients (17.4%) during follow-up. Demographic data, clinical data, and baseline radiographic parameters of the two groups were not significantly different. The postoperative thoracolumbar (TL) or lumbar (L) Cobb angle, LIV translation, and LIV + 1 translation were higher in the adding-on group than those in the no adding-on group, while the postoperative coronal imbalance of the adding-on group was lower than that of the no adding-on group. The level difference of last barely touched vertebra (LBTV) and last substantial touched vertebra (LSTV) with LIV were higher in the adding-on group than in the no adding-on group. Conclusion Postoperative TL/L curve, postoperative LIV translation, postoperative LIV + 1 translation, and postoperative coronal imbalance were determined as risk factors for postoperative distal adding-on in patients with Lenke 5C AIS. Moreover, LIV selection of LBTV-1 or LSTV-1 may cause a higher risk of postoperative distal adding-on.
    Type of Medium: Online Resource
    ISSN: 1471-2474
    URL: Article
    DOI: 10.1186/s12891-022-05559-4
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2041355-5
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  • 2
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    Matrix stiffness induces Drp1-mediated mitochondrial fission through Piezo1 mechanotransduction in human intervertebral disc degeneration
    Springer Science and Business Media LLC ; 2023
    In:  Journal of Translational Medicine Vol. 21, No. 1 ( 2023-10-10)
    Details
    In: Journal of Translational Medicine, Springer Science and Business Media LLC, Vol. 21, No. 1 ( 2023-10-10)
    Abstract: Extracellular matrix stiffness is emerging as a crucial mechanical cue that drives the progression of various diseases, such as cancer, fibrosis, and inflammation. The matrix stiffness of the nucleus pulposus (NP) tissues increase gradually during intervertebral disc degeneration (IDD), while the mechanism through which NP cells sense and react to matrix stiffness remains unclear. In addition, mitochondrial dynamics play a key role in various cellular functions. An in-depth investigation of the pathogenesis of IDD can provide new insights for the development of effective therapies. In this study, we aim to investigate the effects of matrix stiffness on mitochondrial dynamics in IDD. Methods To build the gradient stiffness model, NP cells were cultured on polystyrene plates with different stiffness. Western blot analysis, and immunofluorescence staining were used to detect the expression of mitochondrial dynamics-related proteins. Flow cytometry was used to detect the mitochondrial membrane potential and intracellular Ca 2+ levels. Apoptosis related proteins, ROS level, and TUNEL staining were performed to assess the effect of substrate stiffness on NP cells. Results Stiff substrate increased phosphorylation of dynamin-related protein 1 (Drp1) at Ser616 by activating extracellular signal-regulated kinase 1/2 (ERK1/2) pathway, which promoted mitochondrial fission and apoptosis in NP cells. Furthermore, Piezo1 activation was involved in the regulation of the post-translational modifications of Drp1 and mitochondrial fission caused by matrix stiffness. Inhibition of Piezo1 and ERK1/2 can effectively reduce stiffness-induced ROS elevation and apoptosis in NP cells. Conclusions Our results revealed that stiff substrate causes Piezo1 activation and Ca 2+ influx, results in ERK1/2 activation and phosphorylation of Drp1 at S616, and finally leads to mitochondrial fission and apoptosis in NP cells. These findings reveal a new mechanism of mechanotransduction in NP cells, providing novel insights into the development of therapies for treating IDD.
    Type of Medium: Online Resource
    ISSN: 1479-5876
    URL: Article
    DOI: 10.1186/s12967-023-04590-w
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2118570-0
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  • 3
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    Vasorin-containing small extracellular vesicles retard intervertebral disc degeneration utilizing an injectable thermoresponsive delivery system
    Springer Science and Business Media LLC ; 2022
    In:  Journal of Nanobiotechnology Vol. 20, No. 1 ( 2022-09-19)
    Details
    In: Journal of Nanobiotechnology, Springer Science and Business Media LLC, Vol. 20, No. 1 ( 2022-09-19)
    Abstract: Intervertebral disc degeneration (IDD) is the pathological reason of back pain and the therapeutic approaches are still unsatisfactory. Recently, mesenchymal stem cell-derived small extracellular vesicles (EVs) have emerged as the novel regenerative method for IDD. In this study, we intensively investigated the therapeutic mechanism of small EVs, and found that vasorin protein enriched in EVs promoted the proliferation and extracellular matrix anabolism of nucleus pulposus cells via the Notch1 signaling pathway. Then, we fabricated a thermoresponsive gel which composed of Pluronic F127 and decellularized extracellular matrix (FEC) for the delivery and sustained release of EVs. Besides, ex vivo and in vivo results showed that EVs embedded in FEC (EVs@FEC) ameliorate the disc degeneration efficiently and achieve better therapeutic effects than one-off EVs delivery. Collectively, these findings deepen the understanding of EVs mechanism in treating intervertebral disc degeneration, and also illustrate the promising capacity of sustained EVs release system for intervertebral disc regeneration.
    Type of Medium: Online Resource
    ISSN: 1477-3155
    URL: Article
    DOI: 10.1186/s12951-022-01624-1
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2100022-0
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  • 4
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    Author Correction: WTAP-mediated m6A modification of lncRNA NORAD promotes intervertebral disc degeneration
    Springer Science and Business Media LLC ; 2022
    In:  Nature Communications Vol. 13, No. 1 ( 2022-06-22)
    Details
    In: Nature Communications, Springer Science and Business Media LLC, Vol. 13, No. 1 ( 2022-06-22)
    Type of Medium: Online Resource
    ISSN: 2041-1723
    URL: Article
    DOI: 10.1038/s41467-022-31302-7
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2553671-0
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  • 5
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    Image1.tif
    Frontiers Media SA ; 2021
    In:  Frontiers in Bioengineering and Biotechnology Vol. 9 ( 2021-8-31)
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    In: Frontiers in Bioengineering and Biotechnology, Frontiers Media SA, Vol. 9 ( 2021-8-31)
    Abstract: Symptomatic adjacent segment disease (ASD) is a common challenge after anterior cervical discectomy and fusion (ACDF). The objective of this study was to compare the biomechanical effects of a second ACDF and laminoplasty for the treatment of ASD after primary ACDF. We developed a finite element (FE) model of the C2-T1 based on computed tomography images. The FE models of revision surgeries of ACDF and laminoplasty were simulated to treat one-level and two-level ASD after primary ACDF. The range of motion (ROM) and intradiscal pressure (IDP) of the adjacent segments, and stress in the cord were analyzed to investigate the biomechanical effects of the second ACDF and laminoplasty. The results indicated that revision surgery of one-level ACDF increased the ROM and IDP at the C2–C3 segment, whereas two-level ACDF significantly increased the ROM and IDP at the C2–C3 and C7-T1 segments. Furthermore, no significant changes in the ROM and IDP of the laminoplasty models were observed. The stress in the cord of the re-laminoplasty model decreased to some extent, which was higher than that of the re-ACDF model. In conclusion, both ACDF and laminoplasty can relieve the high level of stress in the spinal cord caused by ASD after primary ACDF, whereas ACDF can achieve better decompression effect. Revision surgery of the superior ACDF or the superior and inferior ACDF after the primary ACDF increased the ROM and IDP at the adjacent segments, which may be the reason for the high incidence of recurrent ASD after second ACDF.
    Type of Medium: Online Resource
    ISSN: 2296-4185
    URL: Article
    URL: Article
    DOI: 10.3389/fbioe.2021.718996
    DOI: 10.3389/fbioe.2021.718996.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2719493-0
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  • 6
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    The distinct roles of myosin IIA and IIB under compression stress in nucleus pulposus cells
    Wiley ; 2021
    In:  Cell Proliferation Vol. 54, No. 2 ( 2021-02)
    Details
    In: Cell Proliferation, Wiley, Vol. 54, No. 2 ( 2021-02)
    Abstract: Inappropriate or excessive compression applied to intervertebral disc (IVD) contributes substantially to IVD degeneration. The actomyosin system plays a leading role in responding to mechanical stimuli. In the present study, we investigated the roles of myosin II isoforms in the compression stress‐induced senescence of nucleus pulposus (NP) cells. Material and methods Nucleus pulposus cells were exposed to 1.0 MPa compression for 0, 12, 24 or 36 hours. Immunofluorescence and co‐immunoprecipitation analysis were used to measure the interaction of myosin IIA and IIB with actin. Western blot analysis and immunofluorescence staining were used to detect nuclear expression and nuclear localization of MRTF‐A. In addition, the expression levels of p‐RhoA/RhoA, ROCK1/2 and p‐MLC/MLC were measured in human NP cells under compression stress and in degenerative IVD tissues. Results Compression stress increased the interaction of myosin IIA and actin, while the interaction of myosin IIB and actin was reduced. The actomyosin cytoskeleton remodelling was involved in the compression stress‐induced fibrotic phenotype mediated by MRTF‐A nuclear translocation and inhibition of proliferation in NP cells. Furthermore, RhoA/ROCK1 pathway activation mediated compression stress‐induced human NP cells senescence by regulating the interaction of myosin IIA and IIB with actin. Conclusions We for the first time investigated the regulation of actomyosin cytoskeleton in human NP cells under compression stress. It provided new insights into the development of therapy for effectively inhibiting IVD degeneration.
    Type of Medium: Online Resource
    ISSN: 0960-7722 , 1365-2184
    URL: Issue
    URL: Article
    DOI: 10.1111/cpr.v54.2
    DOI: 10.1111/cpr.12987
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2019986-7
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  • 7
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    Cytosolic escape of mitochondrial DNA triggers cGAS-STING-NLRP3 axis-dependent nucleus pulposus cell pyroptosis
    Springer Science and Business Media LLC ; 2022
    In:  Experimental & Molecular Medicine Vol. 54, No. 2 ( 2022-02), p. 129-142
    Details
    In: Experimental & Molecular Medicine, Springer Science and Business Media LLC, Vol. 54, No. 2 ( 2022-02), p. 129-142
    Abstract: Low back pain (LBP) is a major musculoskeletal disorder and the socioeconomic problem with a high prevalence that mainly involves intervertebral disc (IVD) degeneration, characterized by progressive nucleus pulposus (NP) cell death and the development of an inflammatory microenvironment in NP tissue. Excessively accumulated cytosolic DNA acts as a damage-associated molecular pattern (DAMP) that is monitored by the cGAS-STING axis to trigger the immune response in many degenerative diseases. NLRP3 inflammasome-dependent pyroptosis is a type of inflammatory programmed death that promotes a chronic inflammatory response and tissue degeneration. However, the relationship between the cGAS-STING axis and NLRP3 inflammasome-induced pyroptosis in the pathogenesis of IVD degeneration remains unclear. Here, we used magnetic resonance imaging (MRI) and histopathology to demonstrate that cGAS, STING, and NLRP3 are associated with the degree of IVD degeneration. Oxidative stress induced cGAS-STING axis activation and NLRP3 inflammasome-mediated pyroptosis in a STING-dependent manner in human NP cells. Interestingly, the canonical morphological and functional characteristics of mitochondrial permeability transition pore (mPTP) opening with the cytosolic escape of mitochondrial DNA (mtDNA) were observed in human NP cells under oxidative stress. Furthermore, the administration of a specific pharmacological inhibitor of mPTP and self-mtDNA cytosolic leakage effectively reduced NLRP3 inflammasome-mediated pyroptotic NP cell death and microenvironmental inflammation in vitro and degenerative progression in a rat disc needle puncture model. Collectively, these data highlight the critical roles of the cGAS-STING-NLRP3 axis and pyroptosis in the progression of IVD degeneration and provide promising therapeutic approaches for discogenic LBP.
    Type of Medium: Online Resource
    ISSN: 1226-3613 , 2092-6413
    URL: Article
    DOI: 10.1038/s12276-022-00729-9
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2084833-X
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  • 8
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    Small extracellular vesicles with nanomorphology memory promote osteogenesis
    Elsevier BV ; 2022
    In:  Bioactive Materials Vol. 17 ( 2022-11), p. 425-438
    Details
    In: Bioactive Materials, Elsevier BV, Vol. 17 ( 2022-11), p. 425-438
    Type of Medium: Online Resource
    ISSN: 2452-199X
    URL: Article
    DOI: 10.1016/j.bioactmat.2022.01.008
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2022
    detail.hit.zdb_id: 2970496-0
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  • 9
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    O-GlcNAc transferase regulates intervertebral disc degeneration by targeting FAM134B-mediated ER-phagy
    Springer Science and Business Media LLC ; 2022
    In:  Experimental & Molecular Medicine Vol. 54, No. 9 ( 2022-09-02), p. 1472-1485
    Details
    In: Experimental & Molecular Medicine, Springer Science and Business Media LLC, Vol. 54, No. 9 ( 2022-09-02), p. 1472-1485
    Abstract: Both O-linked β-N-acetylglucosaminylation (O-GlcNAcylation) and endoplasmic reticulum-phagy (ER-phagy) are well-characterized conserved adaptive regulatory mechanisms that maintain cellular homeostasis and function in response to various stress conditions. Abnormalities in O-GlcNAcylation and ER-phagy have been documented in a wide variety of human pathologies. However, whether O-GlcNAcylation or ER-phagy is involved in the pathogenesis of intervertebral disc degeneration (IDD) is largely unknown. In this study, we investigated the function of O-GlcNAcylation and ER-phagy and the related underlying mechanisms in IDD. We found that the expression profiles of O-GlcNAcylation and O-GlcNAc transferase (OGT) were notably increased in degenerated NP tissues and nutrient-deprived nucleus pulposus (NP) cells. By modulating the O-GlcNAc level through genetic manipulation and specific pharmacological intervention, we revealed that increasing O-GlcNAcylation abundance substantially enhanced cell function and facilitated cell survival under nutrient deprivation (ND) conditions. Moreover, FAM134B-mediated ER-phagy activation was regulated by O-GlcNAcylation, and suppression of ER-phagy by FAM134B knockdown considerably counteracted the protective effects of amplified O-GlcNAcylation. Mechanistically, FAM134B was determined to be a potential target of OGT, and O-GlcNAcylation of FAM134B notably reduced FAM134B ubiquitination-mediated degradation. Correspondingly, the protection conferred by modulating O-GlcNAcylation homeostasis was verified in a rat IDD model. Our data demonstrated that OGT directly associates with and stabilizes FAM134B and subsequently enhances FAM134B-mediated ER-phagy to enhance the adaptive capability of cells in response to nutrient deficiency. These findings may provide a new option for O-GlcNAcylation-based therapeutics in IDD prevention.
    Type of Medium: Online Resource
    ISSN: 2092-6413
    URL: Article
    DOI: 10.1038/s12276-022-00844-7
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
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  • 10
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    Ferroportin-Dependent Iron Homeostasis Protects against Oxidative Stress-Induced Nucleus Pulposus Cell Ferroptosis and Ameliorates Intervertebral Disc Degeneration In Vivo
    Hindawi Limited ; 2021
    In:  Oxidative Medicine and Cellular Longevity Vol. 2021 ( 2021-2-10), p. 1-18
    Details
    In: Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2021 ( 2021-2-10), p. 1-18
    Abstract: Ferroptosis is a specialized form of regulated cell death that is charactered by iron-dependent lethal lipid peroxidation, a process associated with multiple diseases. However, its role in the pathogenesis of intervertebral disc degeneration (IVDD) is rarely investigated. This study is aimed at investigating the role of ferroptosis in oxidative stress- (OS-) induced nucleus pulposus cell (NPC) decline and the pathogenesis of IVDD and determine the underlying regulatory mechanisms. We used tert-butyl hydroperoxide (TBHP) to simulate OS conditions around human NPCs. Flow cytometry and transmission electron microscopy were used to identify ferroptosis, while iron assay kit, Perl’s staining, and western blotting were performed to assay the intracellular iron levels. A ferroportin- (FPN-) lentivirus and FPN-siRNA were constructed and used to explore the relationship between FPN, intracellular iron homeostasis, and ferroptosis. Furthermore, hinokitiol, a bioactive compound known to specifically resist OS and restore FPN function, was evaluated for its therapeutic role in IVDD both in vitro and in vivo. The results indicated that intercellular iron overload plays an essential role in TBHP-induced ferroptosis of human NPCs. Mechanistically, FPN dysregulation is responsible for intercellular iron overload under OS. The increase in nuclear translocation of metal-regulatory transcription factor 1 (MTF1) restored the function of FPN, abolished the intercellular iron overload, and protected cells against ferroptosis. Additionally, hinokitiol enhanced the nuclear translocation of MTF1 by suppressing the JNK pathway and ameliorated the progression of IVDD in vivo. Taken together, our results demonstrate that ferroptosis and FPN dysfunction are involved in the NPC depletion and the pathogenesis of IVDD under OS. To the best of our knowledge, this is the first study to demonstrate the protective role of FPN in ferroptosis of NPCs, suggesting its potential used as a novel therapeutic target against IVDD.
    Type of Medium: Online Resource
    ISSN: 1942-0994 , 1942-0900
    URL: Article
    DOI: 10.1155/2021/6670497
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2021
    detail.hit.zdb_id: 2455981-7
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