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  • 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
    Online Resource
    Online Resource
    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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  • 3
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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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  • 4
    Online Resource
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    Image1.tif
    Frontiers Media SA ; 2021
    In:  Frontiers in Bioengineering and Biotechnology Vol. 9 ( 2021-8-31)
    Details
    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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  • 5
    Online Resource
    Online Resource
    Engineering Extracellular Vesicles Restore the Impaired Cellular Uptake and Attenuate Intervertebral Disc Degeneration
    American Chemical Society (ACS) ; 2021
    In:  ACS Nano Vol. 15, No. 9 ( 2021-09-28), p. 14709-14724
    Details
    In: ACS Nano, American Chemical Society (ACS), Vol. 15, No. 9 ( 2021-09-28), p. 14709-14724
    Type of Medium: Online Resource
    ISSN: 1936-0851 , 1936-086X
    URL: Article
    URL: Article
    DOI: 10.1021/acsnano.1c04514
    DOI: 10.1021/acsnano.1c04514.s001
    Language: English
    Publisher: American Chemical Society (ACS)
    Publication Date: 2021
    detail.hit.zdb_id: 2383064-5
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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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    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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  • 8
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    Online Resource
    Metformin facilitates mesenchymal stem cell-derived extracellular nanovesicles release and optimizes therapeutic efficacy in intervertebral disc degeneration
    Elsevier BV ; 2021
    In:  Biomaterials Vol. 274 ( 2021-07), p. 120850-
    Details
    In: Biomaterials, Elsevier BV, Vol. 274 ( 2021-07), p. 120850-
    Type of Medium: Online Resource
    ISSN: 0142-9612
    URL: Article
    DOI: 10.1016/j.biomaterials.2021.120850
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2021
    detail.hit.zdb_id: 2004010-6
    SSG: 12
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  • 9
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    Online Resource
    Bone-derived mesenchymal stem cells alleviate compression-induced apoptosis of nucleus pulposus cells by N6 methyladenosine of autophagy
    Springer Science and Business Media LLC ; 2020
    In:  Cell Death & Disease Vol. 11, No. 2 ( 2020-02-06)
    Details
    In: Cell Death & Disease, Springer Science and Business Media LLC, Vol. 11, No. 2 ( 2020-02-06)
    Abstract: N6 methyladenosine (m 6 A) is one of the most prevalent epitranscriptomic modifications of mRNAs, and plays a critical role in various bioprocesses. Bone-derived mesenchymal stem cells (BMSCs) can attenuate apoptosis of nucleus pulposus cells (NPCs) under compression; however, the underlying mechanisms are poorly understood. This study showed that the level of m 6 A mRNA modifications was decreased, and the autophagic flux was increased in NPCs under compression when they were cocultured with BMSCs. We report that under coculture conditions, RNA demethylase ALKBH5-mediated FIP200 mRNA demethylation enhanced autophagic flux and attenuated the apoptosis of NPCs under compression. Specific silencing of ALKBH5 results in impaired autophagic flux and a higher proportion of apoptotic NPCs under compression, even when cocultured with BMSCs. Mechanistically, we further identify that the m 6 A “reader” YTHDF2 is likely to be involved in the regulation of autophagy, and lower m 6 A levels in the coding region of FIP200 lead to a reduction in YTHDF2-mediated mRNA degradation of FIP200, a core molecular component of the ULK1 complex that participates in the initiating process of autophagy. Taken together, our study reveals the roles of ALKBH5-mediated FIP200 mRNA demethylation in enhancing autophagy and reducing apoptosis in NPCs when cocultured with BMSCs.
    Type of Medium: Online Resource
    ISSN: 2041-4889
    URL: Article
    DOI: 10.1038/s41419-020-2284-8
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2020
    detail.hit.zdb_id: 2541626-1
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  • 10
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    Selective cargo sorting in stem cell‐derived small extracellular vesicles: impact on therapeutic efficacy for intervertebral disc degeneration
    Wiley ; 2023
    In:  Clinical and Translational Medicine Vol. 13, No. 12 ( 2023-12)
    Details
    In: Clinical and Translational Medicine, Wiley, Vol. 13, No. 12 ( 2023-12)
    Abstract: Growing evidence has suggested the role of stem cell‐derived small extracellular vesicles (sEVs) in intervertebral disc degeneration (IVDD). The cargo sorting of sEVs, particularly miRNAs, may be influenced when the donor cell is subjected to oxidative stress. Here, we discovered that miRNAs containing specific motifs are selectively sorted into intraluminal vesicles within mesenchymal stem cells (MSCs) in response to oxidative stress. Methods Analysis of miRNA cargoes in sEVs derived from normal MSCs (C‐sEVs) or stressed MSCs (T‐sEVs) was conducted using miRNA sequencing. Differential expressed miRNAs in sEVs and the identification of motifs were evaluated through bioinformatics analysis. Protein binding was assessed using immunofluorescent staining and immunoprecipitation analysis. Additionally, RNA pull down and RNA immunoprecipitation (RIP) immunoprecipitation were employed to determine the binding between miRNAs and proteins. The effects of C‐sEVs and T‐sEVs on IVDD were compared by detecting the expression levels of phenotypic genes in vitro or histological evaluation in vivo. Results The sorting process of miRNAs is mediated by the nucleocytoplasmic transport of heterogeneous nuclear ribonucleoproteins, which in turn facilitates the phosphorylation of SNAP25 and promotes the transport and secretion of sEVs. Additionally, CHMP1B plays a role in membrane repair and protects against cell ferroptosis upon oxidative stress, concurrently affecting the release of sEVs. Notably, stem cell‐derived sEVs associated with ferroptosis impair the therapeutic efficacy for IVDD. However, the application of engineered sEVs containing a specific miRNA inhibitor exhibits the potential to reinstate the therapeutic efficacy for IVDD both in vitro and in vivo. Conclusions Taken together, our findings shed light on the mechanism of miRNAs sorting into sEVs and offer new insights for the optimization of sEV‐based treatments during intervertebral disc regeneration. regeneration.
    Type of Medium: Online Resource
    ISSN: 2001-1326 , 2001-1326
    URL: Issue
    URL: Article
    DOI: 10.1002/ctm2.v13.12
    DOI: 10.1002/ctm2.1494
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2697013-2
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