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  • 1
    Online Resource
    Online Resource
    Antibacterial Fusion Protein BPI21/LL-37 Modification Enhances the Therapeutic Efficacy of hUC-MSCs in Sepsis
    Elsevier BV ; 2020
    In:  Molecular Therapy Vol. 28, No. 8 ( 2020-08), p. 1806-1817
    Details
    In: Molecular Therapy, Elsevier BV, Vol. 28, No. 8 ( 2020-08), p. 1806-1817
    Type of Medium: Online Resource
    ISSN: 1525-0016
    URL: Article
    DOI: 10.1016/j.ymthe.2020.05.014
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2020
    detail.hit.zdb_id: 2001818-6
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  • 2
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    Low‐concentration DMSO accelerates skin wound healing by Akt / mTOR ‐mediated cell proliferation and migration in diabetic mice
    Wiley ; 2020
    In:  British Journal of Pharmacology Vol. 177, No. 14 ( 2020-07), p. 3327-3341
    Details
    In: British Journal of Pharmacology, Wiley, Vol. 177, No. 14 ( 2020-07), p. 3327-3341
    Abstract: DMSO has been found to promote tissue repair. However, the role of DMSO in diabetic skin wound healing and the underlying molecular mechanisms are still unclear. Experimental Approach The effects of DMSO on wound healing were evaluated by HE staining, immunohistochemistry and collagen staining using a wound model of full‐thickness skin resection on the backs of non‐diabetic or diabetic mice. Real‐time cell analysis and 5‐ethynyl‐2′‐deoxyuridine incorporation assays were used to study the effect of DMSO on primary fibroblast proliferation. A transwell assay was used to investigate keratinocyte migration. The associated signalling pathway was identified by western blotting and inhibitor blocking. The effect of DMSO on the translation rate of downstream target genes was studied by RT‐qPCR of polyribosome mRNA . Key Results We found that low‐concentration DMSO significantly accelerated skin wound closure by promoting fibroblast proliferation in both nondiabetic and diabetic mice. In addition, increased migration of keratinocytes may also contribute to accelerated wound healing, which was stimulated by increased TGF‐β1 secretion from fibroblasts. Furthermore, we demonstrated that this effect of DMSO depends on Akt/mTOR‐mediated translational control and the promotion of the translation of a set of cell proliferation‐related genes. As expected, DMSO‐induced wound healing and cell proliferation were impaired by rapamycin, an inhibitor of Akt/mTOR signalling. Conclusion and Implications DMSO can promote skin wound healing in diabetic mice by activating the Akt/mTOR pathway. Low‐concentration DMSO presents an alternative medication for chronic cutaneous wounds, especially for diabetic patients.
    Type of Medium: Online Resource
    ISSN: 0007-1188 , 1476-5381
    URL: Issue
    URL: Article
    DOI: 10.1111/bph.v177.14
    DOI: 10.1111/bph.15052
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2029728-2
    SSG: 15,3
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  • 3
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    METTL3/IGF2BP3 axis inhibits tumor immune surveillance by upregulating N6-methyladenosine modification of PD-L1 mRNA in breast cancer
    Springer Science and Business Media LLC ; 2022
    In:  Molecular Cancer Vol. 21, No. 1 ( 2022-12)
    Details
    In: Molecular Cancer, Springer Science and Business Media LLC, Vol. 21, No. 1 ( 2022-12)
    Abstract: Continual expression of PD-L1 in tumor cells is critical for tumor immune escape and host T cell exhaustion, however, knowledge on its clinical benefits through inhibition is limited in breast cancer. N 6 -methyladenosine (m 6 A) plays a crucial role in multiple biological activities. Our study aimed to investigate the regulatory role of the m 6 A modification in PD-L1 expression and immune surveillance in breast cancer. Methods MeRIP-seq and epitranscriptomic microarray identified that PD-L1 is the downstream target of METTL3. MeRIP-qPCR, absolute quantification of m 6 A modification assay, and RIP-qPCR were used to examine the molecular mechanism underlying METTL3/m 6 A/IGF2BP3 signaling axis in PD-L1 expression. B-NDG and BALB/c mice were used to construct xenograft tumor models to verify the phenotypes upon METTL3 and IGF2BP3 silencing. In addition, breast cancer tissue microarray was used to analyze the correlation between PD-L1 and METTL3 or IGF2BP3 expression. Results We identified that PD-L1 was a downstream target of METTL3-mediated m 6 A modification in breast cancer cells. METTL3 knockdown significantly abolished m 6 A modification and reduced stabilization of PD-L1 mRNA. Additionally, METTL3-mediated PD-L1 mRNA activation was m 6 A-IGF2BP3-dependent. Moreover, inhibition of METTL3 or IGF2BP3 enhanced anti-tumor immunity through PD-L1-mediated T cell activation, exhaustion, and infiltration both in vitro and in vivo. PD-L1 expression was also positively correlated with METTL3 and IGF2BP3 expression in breast cancer tissues. Conclusion Our study suggested that METTL3 could post-transcriptionally upregulate PD-L1 expression in an m 6 A-IGF2BP3-dependent manner to further promote stabilization of PD-L1 mRNA, which may have important implications for new and efficient therapeutic strategies in the tumor immunotherapy.
    Type of Medium: Online Resource
    ISSN: 1476-4598
    URL: Article
    DOI: 10.1186/s12943-021-01447-y
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2091373-4
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  • 4
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    TNF-α augments CXCL10/CXCR3 axis activity to induce Epithelial-Mesenchymal Transition in colon cancer cell
    Ivyspring International Publisher ; 2021
    In:  International Journal of Biological Sciences Vol. 17, No. 11 ( 2021), p. 2683-2702
    Details
    In: International Journal of Biological Sciences, Ivyspring International Publisher, Vol. 17, No. 11 ( 2021), p. 2683-2702
    Type of Medium: Online Resource
    ISSN: 1449-2288
    URL: Article
    DOI: 10.7150/ijbs.61350
    Language: English
    Publisher: Ivyspring International Publisher
    Publication Date: 2021
    detail.hit.zdb_id: 2179208-2
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  • 5
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    Anti-αFR CAR-engineered NK-92 Cells Display Potent Cytotoxicity Against αFR-positive Ovarian Cancer
    Ovid Technologies (Wolters Kluwer Health) ; 2019
    In:  Journal of Immunotherapy Vol. 42, No. 8 ( 2019-10), p. 284-296
    Details
    In: Journal of Immunotherapy, Ovid Technologies (Wolters Kluwer Health), Vol. 42, No. 8 ( 2019-10), p. 284-296
    Abstract: Folate receptor alpha (αFR) is overexpressed in 90% of ovarian cancers, one of the most lethal gynecologic cancers. Recent studies have suggested that natural killer (NK) cells may be better chimeric antigen receptor (CAR) drivers because of their favorable innate characteristics, such as directly recognizing and killing tumor cells. However, the therapeutic effects of CAR-engineered NK cells targeting αFR in ovarian cancer have not been reported. In this research, 3 generations of anti-αFR CAR were constructed, namely αFR-ζ (first generation), αFR-28ζ (second generation), and αFR-28BBζ (third generation), and were highly expressed on the surface of NK-92 cells by lentivirus gene transfection. Three anti-αFR CAR-engineered NK-92 cells can specifically kill αFR-positive tumor cells in vitro, especially ovarian cancer cells with high αFR expression. Compared with NK-92 cells expressing αFR-ζ or αFR-28ζ, NK-92 cells expressing αFR-28BBζ showed not only higher antigen-specific cytotoxicity and proliferation but also lower antigen-induced apoptosis. Moreover, stronger degranulation and cytokine secretion were detected in NK-92 cells expressing αFR-28BBζ cocultured with αFR-positive tumor cells. Real-time cell analysis and live cell imaging recorded the process of NK-92 cells expressing αFR-28BBζ killing ovarian cancer cells in vitro. Furthermore, NK-92 cells expressing αFR-28BBζ can effectively eliminate cancer cells in a mouse xenograft model of ovarian cancer and significantly prolong the survival of tumor-bearing mice. These results demonstrate that the anti-αFR CARs redirect NK-92 cells with specific antitumor activity, and the third-generation anti-αFR CAR-engineered NK-92 cells display more potent cytotoxicity against αFR-positive ovarian cancer, laying the foundation for future clinical research.
    Type of Medium: Online Resource
    ISSN: 1524-9557
    URL: Article
    DOI: 10.1097/CJI.0000000000000286
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2019
    detail.hit.zdb_id: 2048797-6
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  • 6
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    Response to: ‘Correspondence to: ‘Combination of human umbilical cord mesenchymal stem cell transplantation with IFN-γ treatment synergistically improves the clinical outcomes of patients with rheumatoid arthritis’’ by Ma et al
    BMJ ; 2022
    In:  Annals of the Rheumatic Diseases Vol. 81, No. 10 ( 2022-10), p. e207-e207
    Details
    In: Annals of the Rheumatic Diseases, BMJ, Vol. 81, No. 10 ( 2022-10), p. e207-e207
    Type of Medium: Online Resource
    ISSN: 0003-4967 , 1468-2060
    URL: Article
    DOI: 10.1136/annrheumdis-2020-218762
    RVK:
    XA 10000
    Language: English
    Publisher: BMJ
    Publication Date: 2022
    detail.hit.zdb_id: 1481557-6
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  • 7
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    B2M is a biomarker associated with immune infiltration in High altitude pulmonary edema
    Bentham Science Publishers Ltd. ; 2023
    In:  Combinatorial Chemistry & High Throughput Screening Vol. 26 ( 2023-05-10)
    Details
    In: Combinatorial Chemistry & High Throughput Screening, Bentham Science Publishers Ltd., Vol. 26 ( 2023-05-10)
    Abstract: High altitude pulmonary edema (HAPE) is a serious mountain sickness with certain mortality. Its early diagnosis is very important. However, the mechanism of its onset and progression is still controversial. Purpose: This study aimed to analyze the HAPE occurrence and development mechanism and search for prospective biomarkers in peripheral blood. Methods: The difference genes (DEGs) of the Control group and the HAPE group were enriched by gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, and then GSEA analysis was performed. After identifying the immune-related hub genes, QPCR was used to verify and analyze the hub gene function and diagnostic value with single-gene GSEA and ROC curves, and the drugs that acted on the hub gene was found in the CTD database. Immune infiltration and its association with the hub genes were analyzed using CIBERSORT. Finally, WGCNA was employed to investigate immune invasion cells' significantly related gene modules, following enrichment analysis of their GO and KEGG. Results: The dataset enrichment analysis, immune invasion analysis and WGCNA analysis showed that the occurrence and early progression of HAPE were unrelated to inflammation. The hub genes associated with immunity obtained with MCODE algorithm of Cytoscape were JAK2 and B2M. RT-qPCR and ROC curves confirmed that the hub gene B2M was a specific biomarker of HAPE and had diagnostic value, and single-gene GSEA analysis confirmed that it participated in MHC I molecule-mediated antigen presentation ability decreased, resulting in reduced immunity. Conclusion: Occurrence and early progression of high altitude pulmonary edema may not be related to inflammation. B2M may be a new clinical potential biomarker for HAPE for early diagnosis and therapeutic evaluation as well as therapeutic targets, and its decrease may be related to reduced immunity due to reduced ability of MCH I to participate in antigen submission.
    Type of Medium: Online Resource
    ISSN: 1386-2073
    URL: Article
    DOI: 10.2174/1386207326666230510095840
    Language: English
    Publisher: Bentham Science Publishers Ltd.
    Publication Date: 2023
    SSG: 15,3
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  • 8
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    Online Resource
    Combination of human umbilical cord mesenchymal stem (stromal) cell transplantation with IFN-γ treatment synergistically improves the clinical outcomes of patients with rheumatoid arthritis
    BMJ ; 2020
    In:  Annals of the Rheumatic Diseases Vol. 79, No. 10 ( 2020-10), p. 1298-1304
    Details
    In: Annals of the Rheumatic Diseases, BMJ, Vol. 79, No. 10 ( 2020-10), p. 1298-1304
    Abstract: To clarify the key role of circulating interferon-γ (IFN-γ) and to improve the clinical efficacy of mesenchymal stem cell (MSC) transplantation (MSCT) in patients with rheumatoid arthritis (RA). Methods Study of wild-type or IFN-γR -/- MSCT was first evaluated in a murine model of collagen-induced arthritis (CIA) following which a phase 1/2 randomised controlled study was conducted in 63 patients with RA who responded poorly to regular clinical treatments. Subjects were randomly assigned to an MSCT monotherapy group (n=32) or an MSCT plus recombinant human IFN-γ treatment group (n=31), with 1 year of follow-up. The primary end points consisted of efficacy as assessed as good or moderate EULAR response rates and the proportion of patients at 3 months attaining American College of Rheumatology 20 (ACR20) response rates. Results In the murine studies, wild-type MSCT significantly improved the clinical severity of CIA, while IFN-γR -/- MSCT aggravated synovitis, and joint and cartilage damage. Transitioning from the murine to the clinical study, the 3-month follow-up results showed that the efficacy and ACR20 response rates were attained in 53.3% patients with MSCT monotherapy and in 93.3% patients with MSCT combined with IFN-γ treatment (p 〈 0.05). No new or unexpected safety issues were encountered in 1-year follow-up for either treatment group. Conclusions The results of this study show that IFN-γ is a key factor in determining the efficacy of MSCT in the treatment of RA, and that an MSC plus IFN-γ combination therapeutic strategy can greatly improve the clinical efficacy of MSC-based therapy in RA patients.
    Type of Medium: Online Resource
    ISSN: 0003-4967 , 1468-2060
    URL: Article
    DOI: 10.1136/annrheumdis-2020-217798
    RVK:
    XA 10000
    Language: English
    Publisher: BMJ
    Publication Date: 2020
    detail.hit.zdb_id: 1481557-6
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  • 9
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    Online Resource
    Cross talk between glucose metabolism and immunosuppression in IFN-γ–primed mesenchymal stem cells
    Life Science Alliance, LLC ; 2022
    In:  Life Science Alliance Vol. 5, No. 12 ( 2022-12), p. e202201493-
    Details
    In: Life Science Alliance, Life Science Alliance, LLC, Vol. 5, No. 12 ( 2022-12), p. e202201493-
    Abstract: The immunosuppressive function “licensed” by IFN-γ is a vital attribute of mesenchymal stem cells (MSCs) widely used in the treatment of inflammatory diseases. However, the mechanism and impact of metabolic reprogramming on MSC immunomodulatory plasticity remain unclear. Here, we explored the mechanism by which glucose metabolism affects the immunomodulatory reprogramming of MSCs “licensed” by IFN-γ. Our data showed that glucose metabolism regulates the immunosuppressive function of human umbilical cord MSCs (hUC-MSCs) challenged by IFN-γ through the Janus kinase–signal transducer and activator of transcription (JAK-STAT) pathway. Furthermore, ATP facilitated the cross talk between glucose metabolism and the JAK-STAT system, which stimulates the phosphorylation of JAK2 and STATs, as well as the expression of indoleamine 2, 3-dioxygenase and programmed cell death-1 ligand. Moreover, ATP synergistically enhanced the therapeutic efficacy of IFN-γ–primed hUC-MSCs against acute pneumonia in mice. These results indicate a novel cross talk between the immunosuppressive function, glucose metabolism, and mitochondrial oxidation and provide a novel targeting strategy to enhance the therapeutic efficacies of hUC-MSCs.
    Type of Medium: Online Resource
    ISSN: 2575-1077
    URL: Article
    DOI: 10.26508/lsa.202201493
    Language: English
    Publisher: Life Science Alliance, LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2948687-7
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  • 10
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    Opposing Roles of Wnt Inhibitors IGFBP-4 and Dkk1 in Cardiac Ischemia by Differential Targeting of LRP5/6 and β-catenin
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Circulation Vol. 134, No. 24 ( 2016-12-13), p. 1991-2007
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 134, No. 24 ( 2016-12-13), p. 1991-2007
    Abstract: Myocardial infarction is one of the leading causes of morbidity and mortality worldwide, triggering irreversible myocardial cell damage and heart failure. The role of low-density lipoprotein receptor-related proteins 5 and 6 (LRP5/6) as coreceptors of the Wnt/β-catenin pathway in the adult heart remain unknown. Insulin-like growth factor binding protein 4 and dickkopf-related protein 1 (Dkk1) are 2 secreted LRP5/6 binding proteins that play a crucial role in heart development through preventing Wnt/β-catenin pathway activation. However, their roles in the adult heart remain unexplored. Methods: To understand the role of LRP5/6 and β-catenin in the adult heart, we constructed conditional cardiomyocyte-specific LRP5/6 and β-catenin knockout mice and induced surgical myocardial infarction. We also directly injected recombinant proteins of insulin-like growth factor binding protein 4 and Dkk1 into the heart immediately following myocardial infarction to further examine the mechanisms through which these proteins regulate LRP5/6 and β-catenin. Results: Deletion of LRP5/6 promoted cardiac ischemic insults. Conversely, deficiency of β-catenin, a downstream target of LRP5/6, was beneficial in ischemic injury. It is interesting to note that although both insulin-like growth factor binding protein 4 and Dkk1 are secreted Wnt/β-catenin pathway inhibitors, insulin-like growth factor binding protein 4 protected the ischemic heart by inhibiting β-catenin, whereas Dkk1 enhanced the injury response mainly through inducing LRP5/6 endocytosis and degradation. Conclusions: Our findings reveal previously unidentified dual roles of LRP5/6 involved in the cardiomyocyte response to ischemic injury. These findings suggest new therapeutic strategies in ischemic heart disease by fine-tuning LRP5/6 and β-catenin signaling within the Wnt/β-catenin pathway.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/CIRCULATIONAHA.116.024441
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 1466401-X
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