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  1. Article ; Online: Neutrophil extracellular traps induce pyroptosis of pulmonary microvascular endothelial cells by activating the NLRP3 inflammasome.

    Zhao, Peipei / Zhu, Jiarui / Bai, Ling / Ma, Wenlan / Li, Feifei / Zhang, Cen / Zhao, Liangtao / Wang, Liuyang / Zhang, Sigong

    Clinical and experimental immunology

    2024  

    Abstract: Excessive formation of neutrophil extracellular traps (NETs) may lead to myositis-related interstitial lung disease (ILD). There is evidence that NETs can directly injure vascular endothelial cells and play a pathogenic role in the inflammatory exudation ...

    Abstract Excessive formation of neutrophil extracellular traps (NETs) may lead to myositis-related interstitial lung disease (ILD). There is evidence that NETs can directly injure vascular endothelial cells and play a pathogenic role in the inflammatory exudation of ILD. However, the specific mechanism is unclear. This study aimed to investigate the specific mechanism underlying NET-induced injury to human pulmonary microvascular endothelial cells (HPMECs). HPMECs were stimulated with NETs (200 ng/ml) in vitro. Cell death was detected by propidium iodide staining. The morphological changes of the cells were observed by transmission electron microscopy (TEM). Pyroptosis markers were detected by western blot, immunofluorescence and quantitative real-time PCR, and the related inflammatory factor IL-1β was verified by ELISA. Compared with the control group, HPMECs mortality increased after NET stimulation, and the number of pyroptosis vacuoles in HPMECs was further observed by TEM. The pulmonary microvascular endothelial cells (PMECs) of the experimental autoimmune myositis (EAM) mouse model also showed a trend of pyroptosis in vivo. Cell experiment further confirmed the significantly high expression of the NLRP3 inflammasome and pyroptosis-related markers, including GSDMD and inflammatory factor IL-1β. Pretreated with the NLRP3 inhibitor MCC950, the activation of NLRP3 inflammasome and pyroptosis of HPMECs were effectively inhibited. Our study confirmed that NETs promote pulmonary microvascular endothelial pyroptosis by activating the NLRP3 inflammasome, suggesting that NETs-induced pyroptosis of PMECs may be a potential pathogenic mechanism of inflammatory exudation in ILD.
    Language English
    Publishing date 2024-03-22
    Publishing country England
    Document type Journal Article
    ZDB-ID 218531-3
    ISSN 1365-2249 ; 0009-9104 ; 0964-2536
    ISSN (online) 1365-2249
    ISSN 0009-9104 ; 0964-2536
    DOI 10.1093/cei/uxae028
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  2. Article ; Online: The role of neutrophil extracellular traps and proinflammatory damage-associated molecular patterns in idiopathic inflammatory myopathies.

    Ma, Wenlan / Zhu, Jiarui / Bai, Ling / Zhao, Peipei / Li, Feifei / Zhang, Sigong

    Clinical and experimental immunology

    2023  Volume 213, Issue 2, Page(s) 202–208

    Abstract: Idiopathic inflammatory myopathies (IIMs) are a group of systemic autoimmune diseases characterized by immune-mediated muscle injury. Abnormal neutrophil extracellular traps (NETs) can be used as a biomarker of IIM disease activity, but the mechanism of ... ...

    Abstract Idiopathic inflammatory myopathies (IIMs) are a group of systemic autoimmune diseases characterized by immune-mediated muscle injury. Abnormal neutrophil extracellular traps (NETs) can be used as a biomarker of IIM disease activity, but the mechanism of NET involvement in IIMs needs to be elucidated. Important components of NETs, including high-mobility group box 1, DNA, histones, extracellular matrix, serum amyloid A, and S100A8/A9, act as damage-associated molecular patterns (DAMPs) to promote inflammation in IIMs. NETs can act on different cells to release large amounts of cytokines and activate the inflammasome, which can subsequently aggravate the inflammatory response. Based on the idea that NETs may be proinflammatory DAMPs of IIMs, we describe the role of NETs, DAMPs, and their interaction in the pathogenesis of IIMs and discuss the possible targeted treatment strategies in IIMs.
    MeSH term(s) Humans ; Extracellular Traps ; Neutrophils ; Myositis/pathology ; Histones ; Inflammation/pathology ; Alarmins
    Chemical Substances Histones ; Alarmins
    Language English
    Publishing date 2023-06-06
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218531-3
    ISSN 1365-2249 ; 0009-9104 ; 0964-2536
    ISSN (online) 1365-2249
    ISSN 0009-9104 ; 0964-2536
    DOI 10.1093/cei/uxad059
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Neutrophil extracellular traps are involved in the occurrence of interstitial lung disease in a murine experimental autoimmune myositis model.

    Bai, Ling / Zhu, Jiarui / Ma, Wenlan / Li, Feifei / Zhao, Peipei / Zhang, Sigong

    Clinical and experimental immunology

    2023  Volume 215, Issue 2, Page(s) 126–136

    Abstract: The excessive formation of neutrophil extracellular traps (NETs) has been demonstrated to be a pathogenic mechanism of idiopathic inflammatory myopathy (IIM)-associated interstitial lung disease (ILD). This study aimed to answer whether an experimental ... ...

    Abstract The excessive formation of neutrophil extracellular traps (NETs) has been demonstrated to be a pathogenic mechanism of idiopathic inflammatory myopathy (IIM)-associated interstitial lung disease (ILD). This study aimed to answer whether an experimental autoimmune myositis (EAM) model can be used to study IIM-ILD and whether NETs participate in the development of EAM-ILD. An EAM mouse model was established using skeletal muscle homogenate and pertussis toxin (PTX). The relationship between NETs and the ILD phenotype was determined via histopathological analysis. As NETs markers, serum cell-free DNA (cfDNA) and serum citrullinated histone 3 (Cit-H3)-DNA were tested. The healthy mouse was injected with PTX intraperitoneally to determine whether PTX intervention could induce NETs formation in vivo. Neutrophils isolated from the peripheral blood of healthy individuals were given different interventions to determine whether PTX and skeletal muscle homogenate can induce neutrophils to form NETs in vitro. EAM-ILD had three pathological phenotypes similar to IIM-ILD. Cit-H3, neutrophil myeloperoxidase, and neutrophil elastase were overexpressed in the lungs of EAM model mice. The serum cfDNA level and Cit-H3-DNA complex level were significantly increased in EAM model mice. Serum cfDNA levels were increased significantly in vivo intervention with PTX in mice. Both PTX and skeletal muscle homogenate-induced neutrophils to form NETs in vitro. EAM-ILD pathological phenotypes are similar to IIM-ILD, and NETs are involved in the development of ILD in a murine model of EAM. Thus, the EAM mouse model can be used as an ideal model targeting NETs to prevent and treat IIM-ILD.
    MeSH term(s) Mice ; Animals ; Extracellular Traps ; Lung Diseases, Interstitial ; Neutrophils ; Histones ; Nervous System Autoimmune Disease, Experimental/pathology ; Disease Models, Animal ; Cell-Free Nucleic Acids ; DNA ; Myositis
    Chemical Substances Histones ; Cell-Free Nucleic Acids ; DNA (9007-49-2)
    Language English
    Publishing date 2023-09-06
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218531-3
    ISSN 1365-2249 ; 0009-9104 ; 0964-2536
    ISSN (online) 1365-2249
    ISSN 0009-9104 ; 0964-2536
    DOI 10.1093/cei/uxad104
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Free Transverse Vibration of Rectangular Orthotropic Plates with Two Opposite Edges Rotationally Restrained and Remaining Others Free

    Yuan Zhang / Sigong Zhang

    Applied Sciences, Vol 9, Iss 1, p

    2018  Volume 22

    Abstract: Many types of engineering structures can be effectively modelled as orthotropic plates with opposite free edges such as bridge decks. The other two edges, however, are usually treated as simply supported or fully clamped in current design practice, ... ...

    Abstract Many types of engineering structures can be effectively modelled as orthotropic plates with opposite free edges such as bridge decks. The other two edges, however, are usually treated as simply supported or fully clamped in current design practice, although the practical boundary conditions are intermediate between these two limiting cases. Frequent applications of orthotropic plates in structures have generated the need for a better understanding of the dynamic behaviour of orthotropic plates with non-classical boundary conditions. In the present study, the transverse vibration of rectangular orthotropic plates with two opposite edges rotationally restrained with the remaining others free was studied by applying the method of finite integral transforms. A new alternative formulation was developed for vibration analysis, which provides much easier solutions. Exact series solutions were derived, and the excellent accuracy and efficiency of the method are demonstrated through considerable numerical studies and comparisons with existing results. Some new results have been presented. In addition, the effect of different degrees of rotational restraints on the mode shapes was also demonstrated. The present analytical method is straightforward and systematic, and the derived characteristic equation for eigenvalues can be easily adapted for broad applications.
    Keywords rectangular orthotropic plate ; transverse vibration ; finite integral transform ; rotationally restrained edges ; free edges ; rotational fixity factors ; Technology ; T ; Engineering (General). Civil engineering (General) ; TA1-2040 ; Biology (General) ; QH301-705.5 ; Physics ; QC1-999 ; Chemistry ; QD1-999
    Subject code 690
    Language English
    Publishing date 2018-12-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Corrigendum to 'Hydroxychloroquine inhibiting neutrophil extracellular trap formation alleviates hepatic ischemia/reperfusion by blocking TLR9 in mice' [Clinical Immunology 216 (2020) 108461].

    Zhang, Sigong / Zhang, Qiuyue / Wang, Furong / Guo, Xuehui / Liu, Tao / Zhao, Yang / Gu, Baohong / Chen, Hao / Li, Yumin

    Clinical immunology (Orlando, Fla.)

    2021  Volume 225, Page(s) 108681

    Language English
    Publishing date 2021-02-03
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 1459903-x
    ISSN 1521-7035 ; 1521-6616
    ISSN (online) 1521-7035
    ISSN 1521-6616
    DOI 10.1016/j.clim.2021.108681
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  6. Article: Upregulation of family with sequence similarity 83 member D expression enhances cell proliferation and motility via activation of Wnt/β-catenin signaling and predicts poor prognosis in gastric cancer.

    Wang, Furong / Zhang, Sigong / Wei, Yucai / Chen, Hao / Jiao, Zuoyi / Li, Yumin

    Cancer management and research

    2019  Volume 11, Page(s) 6775–6791

    Abstract: Background/aims: Gastric cancer (GC) is the third most common cause of cancer-related death worldwide. The molecular mechanisms underlying the progression of gastric cancer are still not fully elucidated. In this study, we focused on exploring the role ... ...

    Abstract Background/aims: Gastric cancer (GC) is the third most common cause of cancer-related death worldwide. The molecular mechanisms underlying the progression of gastric cancer are still not fully elucidated. In this study, we focused on exploring the role of family with sequence similarity 83, member D (FAM83D) in gastric cancer progression.
    Methods: The expression of FAM83D in GC tissues was detected by immunohistochemistry (IHC) staining. FAM83D knockdown or overexpression were constructed in AGS and SGC-7901 cells with two distinct siRNA duplexes and lentivirus infection, respectively, to explore the role of FAM83D in gastric cancer progression. Nude mouse xenograft assay was used to further explore the role of FAM83D in tumorigenesis in vivo.
    Results: We found that FAM83D mRNA and protein levels were higher in human GC tumor tissues and in GC cell lines, compared with the adjacent normal tissues and non-malignant gastric epithelial cell lines, respectively, and that higher FAM83D expression was correlated with worse overall survival (
    Conclusions: This study suggested that FAM83D overexpression enhanced the proliferation, clonogenicity, and motility of GC cells by activating Wnt/β-catenin signaling, and FAM83D may be a promising diagnostic and therapeutic target for human GC.
    Language English
    Publishing date 2019-07-22
    Publishing country New Zealand
    Document type Journal Article
    ZDB-ID 2508013-1
    ISSN 1179-1322
    ISSN 1179-1322
    DOI 10.2147/CMAR.S203082
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  7. Article ; Online: Hydroxychloroquine inhibiting neutrophil extracellular trap formation alleviates hepatic ischemia/reperfusion injury by blocking TLR9 in mice.

    Zhang, Sigong / Zhang, Qiuyue / Wang, Furong / Guo, Xuehui / Liu, Tao / Zhao, Yang / Gu, Baohong / Chen, Hao / Li, Yumin

    Clinical immunology (Orlando, Fla.)

    2020  Volume 216, Page(s) 108461

    Abstract: Hepatic ischemia/reperfusion (I/R) injury may arise after partial hepatectomy and liver transplantation. Neutrophil extracellular traps (NETs) were involved in hepatic I/R injury. This study tested the hypothesis that blocking NETs formation could be a ... ...

    Abstract Hepatic ischemia/reperfusion (I/R) injury may arise after partial hepatectomy and liver transplantation. Neutrophil extracellular traps (NETs) were involved in hepatic I/R injury. This study tested the hypothesis that blocking NETs formation could be a potential therapeutic target against hepatic I/R injury. NETs were excessively formed within liver and in serum of I/R mice models and were testified to be an independent contributor to hepatic I/R injury. Hydroxychloroquine (HCQ) alleviated hepatic I/R injury by inhibiting NETs formation in SCID and c57BL/6 mice models. In vitro, HCQ inhibited neutrophils to form NETs at a concentration of 100 μg/ml. CpG-ODN reversed the effect of HCQ inhibiting NETs formation. HCQ inhibited PAD4 and Rac2 expressions by blocking TLR9. NETs are essential contributors to hepatic I/R injury. HCQ blocking TLR9 protects against hepatic I/R injury by inhibiting NETs formation, which may suggest utility of HCQ or other TLR9 agonists for preventing hepatic I/R injury in clinical practices.
    MeSH term(s) Animals ; Disease Models, Animal ; Extracellular Traps/drug effects ; Extracellular Traps/metabolism ; Hydroxychloroquine/pharmacology ; Liver/drug effects ; Liver/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, SCID ; Neutrophils/drug effects ; Neutrophils/metabolism ; Protein-Arginine Deiminase Type 4/metabolism ; Reperfusion Injury/drug therapy ; Reperfusion Injury/metabolism ; Toll-Like Receptor 9/metabolism ; rac GTP-Binding Proteins/metabolism ; RAC2 GTP-Binding Protein
    Chemical Substances Tlr9 protein, mouse ; Toll-Like Receptor 9 ; Hydroxychloroquine (4QWG6N8QKH) ; Protein-Arginine Deiminase Type 4 (EC 3.5.3.15) ; rac GTP-Binding Proteins (EC 3.6.5.2)
    Language English
    Publishing date 2020-05-11
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1459903-x
    ISSN 1521-7035 ; 1521-6616
    ISSN (online) 1521-7035
    ISSN 1521-6616
    DOI 10.1016/j.clim.2020.108461
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  8. Article ; Online: Abnormally increased low-density granulocytes in peripheral blood mononuclear cells are associated with interstitial lung disease in dermatomyositis.

    Zhang, Sigong / Shen, Haili / Shu, Xiaoming / Peng, Qinglin / Wang, Guochun

    Modern rheumatology

    2017  Volume 27, Issue 1, Page(s) 122–129

    Abstract: Objective: We previously found that neutrophil extracellular traps (NETs) were associated with interstitial lung disease (ILD) in dermatomyositis (DM) patients. However, it is unclear whether low-density granulocytes (LDGs), endowed with enhanced NET ... ...

    Abstract Objective: We previously found that neutrophil extracellular traps (NETs) were associated with interstitial lung disease (ILD) in dermatomyositis (DM) patients. However, it is unclear whether low-density granulocytes (LDGs), endowed with enhanced NET formation capabilities, contribute to the pathogenesis of ILD. This study aims to elucidate the relationship between LDGs and DM-associated ILD.
    Methods: We recruited 48 DM patients (28 with ILD) as well as 19 healthy volunteers for this study. The percentage of LDGs in peripheral blood mononuclear cells (PBMCs) was ascertained by flow cytometry. Plasma cfDNA was measured by using the Quant-iT PicoGreen dsDNA Kit and plasma LL-37 was tested by using the LL-37 ELISA kit.
    Results: The percentage of LDGs was 7.1 times higher in DM patients than in healthy controls. LDG percentage was 2.7 times higher in DM patients with ILD than in DM patients without ILD. Additionally, LDG percentage positively correlated with MYOACT lung disease activity scores, and NET/neutrophil-related marker levels (LL-37, cfDNA, MPO, and MMP-8) in the DM group were significantly higher than those in the control group.
    Conclusion: The abnormal increase of LDGs may exacerbate abnormal NET regulation and further contribute to the pathogenesis of ILD in DM patients by abnormally forming NETs.
    MeSH term(s) Adult ; Biomarkers/blood ; Dermatomyositis/blood ; Dermatomyositis/complications ; Female ; Flow Cytometry ; Granulocytes/pathology ; Humans ; Leukocytes, Mononuclear/pathology ; Lung Diseases, Interstitial/blood ; Lung Diseases, Interstitial/complications ; Male ; Middle Aged
    Chemical Substances Biomarkers
    Language English
    Publishing date 2017-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2078157-X
    ISSN 1439-7609 ; 1439-7595
    ISSN (online) 1439-7609
    ISSN 1439-7595
    DOI 10.1080/14397595.2016.1179861
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  9. Article ; Online: Correction to: identification of multiple cancer-associated myositis-specific autoantibodies in idiopathic inflammatory myopathies: a large longitudinal cohort study.

    Yang, Hanbo / Peng, Qinglin / Yin, Liguo / Li, Shanshan / Shi, Jingli / Zhang, Yamei / Lu, Xin / Shu, Xiaoming / Zhang, Sigong / Wang, Guochun

    Arthritis research & therapy

    2018  Volume 20, Issue 1, Page(s) 71

    Abstract: After publication of the article [1], it has been brought to our attention that the labels in Fig. 2b have been switched and are as a result incorrect. The label for the red line should have the label "non-CAM" and the yellow line "CAM". ...

    Abstract After publication of the article [1], it has been brought to our attention that the labels in Fig. 2b have been switched and are as a result incorrect. The label for the red line should have the label "non-CAM" and the yellow line "CAM".
    Language English
    Publishing date 2018-04-11
    Publishing country England
    Document type Journal Article ; Published Erratum
    ZDB-ID 2107602-9
    ISSN 1478-6362 ; 1478-6354
    ISSN (online) 1478-6362
    ISSN 1478-6354
    DOI 10.1186/s13075-018-1549-4
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  10. Article ; Online: Neutrophil extracellular traps activate lung fibroblast to induce polymyositis-related interstitial lung diseases via TLR9-miR-7-Smad2 pathway.

    Zhang, Sigong / Jia, Xueqin / Zhang, Qiuyue / Zhang, Li / Yang, Jing / Hu, Caihong / Shi, Junnian / Jiang, Xiao / Lu, Jinyue / Shen, Haili

    Journal of cellular and molecular medicine

    2019  Volume 24, Issue 2, Page(s) 1658–1669

    Abstract: Excessive neutrophil extracellular trap (NET) formation may contribute to polymyositis (PM)-associated interstitial lung diseases (ILD), but the underlying mechanism is not fully revealed. In this study, we found that NET accelerated the progression of ... ...

    Abstract Excessive neutrophil extracellular trap (NET) formation may contribute to polymyositis (PM)-associated interstitial lung diseases (ILD), but the underlying mechanism is not fully revealed. In this study, we found that NET accelerated the progression of ILD and promoted pulmonary fibrosis (PF) in vivo. miR-7 expression was down-regulated in lung tissue of PM group than control group, and NETs further decreased miR-7 expression. TLR9 and Smad2 were up-regulated in lung tissue of PM group than control group, and NETs further increased TLR9 and Smad2 expressions. In vitro experiments showed that PMA-treated NETs accelerated the proliferation of LF and their differentiation into myofibroblast (MF), whereas DNase I decreased the promotion effect of NETs. Neutrophil extracellular trap components myeloperoxidase (MPO) and histone 3 also promoted the proliferation and differentiation of LF. In addition, we demonstrated that TLR9 involved in the regulation of NETs on LF proliferation and differentiation, and confirmed the interaction between miR-7 and Smad2 in LF. Finally, miR-7-Smad2 pathway was confirmed to be involved in the regulation of TLR9 on LF proliferation and differentiation. Therefore, NETs promote PM-related ILD, and TLR9-miR-7-Smad2 signalling pathway is involved in the proliferation of LFs and their differentiation into MFs.
    MeSH term(s) Animals ; Base Sequence ; Cell Differentiation ; Cell Proliferation ; Disease Progression ; Extracellular Traps/metabolism ; Female ; Fibroblasts/metabolism ; Histones/metabolism ; Humans ; Lung/pathology ; Mice, Inbred BALB C ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Myofibroblasts/pathology ; Peroxidase/metabolism ; Polymyositis/pathology ; Rats, Sprague-Dawley ; Signal Transduction ; Smad2 Protein/metabolism ; Toll-Like Receptor 9/metabolism
    Chemical Substances Histones ; MIRN7 microRNA, mouse ; MicroRNAs ; Smad2 Protein ; Toll-Like Receptor 9 ; Peroxidase (EC 1.11.1.7)
    Language English
    Publishing date 2019-12-10
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2074559-X
    ISSN 1582-4934 ; 1582-4934 ; 1582-1838
    ISSN (online) 1582-4934
    ISSN 1582-4934 ; 1582-1838
    DOI 10.1111/jcmm.14858
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