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  • 1
    Online Resource
    Online Resource
    Danthron attenuates experimental atherosclerosis by targeting foam cell formation
    Wiley ; 2021
    In:  Experimental Physiology Vol. 106, No. 3 ( 2021-03), p. 653-662
    Details
    In: Experimental Physiology, Wiley, Vol. 106, No. 3 ( 2021-03), p. 653-662
    Abstract: What is the central question of this study? Does danthron alleviate experimental atherosclerosis by inhibiting the formation of foam cells? What are the main findings and their importance? Danthron improved serum lipid profiles and significantly reduced the atherosclerotic plaque areas and lipid accumulation in the aortic root of ApoE −/− mice. Danthron inhibited foam cell formation in oxidized low‐density lipoprotein‐induced RAW264.7 macrophages. Furthermore, danthron exerted its function in atherosclerosis at least partly through activating the AMP‐activated protein kinase–sirtuin 1 signalling pathway. These findings suggest that danthron has the potential to alleviate atherosclerosis. Abstract Danthron, an ingredient isolated from Rheum palmatum L., has been revealed to reduce lipid accumulation in vitro . This study aimed to discover the effects of danthron on the development of atherosclerosis and to delineate the underlying mechanisms. For in vivo studies, male ApoE −/− mice were fed a high‐fat diet and orally treated with danthron (30 or 60 mg/kg/day) for 12 weeks. For in vitro studies, RAW264.7 cells were induced by oxidized low‐density lipoprotein (ox‐LDL, 50 μg/ml) for 48 h and subsequently administered danthron at appropriate concentrations for 24 h. AMP‐activated protein kinase (AMPK) inhibitor compound C was added to ox‐LDL‐stimulated RAW264.7 cells 2 h before danthron administration to confirm the role of the AMPK signalling pathway in the regulation by danthron of foam cell formation. We found that danthron improved serum lipid profiles, and significantly reduced atherosclerotic plaque areas and lipid accumulation in the aortic root of atherosclerotic mice. Moreover, danthron upregulated the mRNA and protein expression of ATP‐binding cassette transporter A1 (ABCA1), ABCG1 and liver X receptor α (LXRα), which play a crucial role in lipid metabolism, and activated the AMPK–sirtuin 1 (SIRT1) pathway. In an in vitro study, danthron inhibited foam cell formation in ox‐LDL‐induced RAW264.7 macrophages with an increase in the expression of ABCA1, ABCG1 and LXRα as well as activation of the AMPK–SIRT1 pathway. Furthermore, compound C abolished the effects of danthron on lipid accumulation and the protein expression of ABCA1/G1 and LXRα in vitro . Our results highlight that danthron possesses potential benefits in alleviating experimental atherosclerosis by targeting foam cell formation by activating the AMPK–SIRT1 signalling pathway.
    Type of Medium: Online Resource
    ISSN: 0958-0670 , 1469-445X
    URL: Issue
    URL: Article
    DOI: 10.1113/eph.v106.3
    DOI: 10.1113/EP089021
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 1493802-9
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  • 2
    Online Resource
    Online Resource
    Higher Percentage of CD3+CD154+ T Lymphocytes Predicts Efficacy of TNF-α Inhibitors in Active Axial SpA Patients
    Springer Science and Business Media LLC ; 2014
    In:  Inflammation Vol. 37, No. 6 ( 2014-12), p. 2056-2061
    Details
    In: Inflammation, Springer Science and Business Media LLC, Vol. 37, No. 6 ( 2014-12), p. 2056-2061
    Type of Medium: Online Resource
    ISSN: 0360-3997 , 1573-2576
    URL: Article
    DOI: 10.1007/s10753-014-9938-6
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2014
    detail.hit.zdb_id: 2015610-8
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  • 3
    Online Resource
    Online Resource
    Tryptanthrin Regulates Vascular Smooth Muscle Cell Phenotypic Switching in Atherosclerosis by AMP-Activated Protein Kinase/Acetyl-CoA Carboxylase Signaling Pathway
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Journal of Cardiovascular Pharmacology Vol. 77, No. 5 ( 2021-05), p. 642-649
    Details
    In: Journal of Cardiovascular Pharmacology, Ovid Technologies (Wolters Kluwer Health), Vol. 77, No. 5 ( 2021-05), p. 642-649
    Abstract: Atherosclerosis (AS) is one of the most severe cardiovascular diseases involved in the phenotypic switching of vascular smooth muscle cells (VSMCs). Tryptanthrin is a natural product with broad biological activities. However, the effect of tryptanthrin on atherosclerotic progression is unclear. The aim of this study was to determine the role of tryptanthrin in AS and explore the potential mechanism. In vitro, primary VSMCs were stimulated with platelet-derived growth factor-BB (PDGF) to induce cell dedifferentiation. Treatment with tryptanthrin (5 μM or 10 μM) suppressed the proliferation and recovered the contractility of VSMCs in the presence of PDGF. The contractile proteins (α-smooth muscle actin, calponin, and SM22α) were increased, and the synthetic protein vimentin was decreased by tryptanthrin in PDGF-induced VSMCs. ApoE −/− mice fed with high-fat diet were used as an in vivo model of AS. Similarly, gavage administration of tryptanthrin (50 mg/kg or 100 mg/kg) attenuated VSMC phenotypic changes from a contractile to a synthetic state in aortic tissues of AS mice. The serum lipid level, atherosclerotic plaque formation, and arterial intimal hyperplasia were attenuated by tryptanthrin. Furthermore, tryptanthrin increased the expression levels of phosphorylated AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) both in vitro and in vivo. Administration of compound C, an AMPK inhibitor, reversed the inhibitory effect of tryptanthrin on VSMC dedifferentiation in vitro. Thus, we demonstrate that tryptanthrin protects against AS progression through the inhibition of VSMC switching from a contractile to a pathological synthetic phenotype by the activation of AMPK/ACC pathway. It provides novel insights into AS prevention and treatment.
    Type of Medium: Online Resource
    ISSN: 0160-2446
    URL: Article
    DOI: 10.1097/FJC.0000000000001008
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 2049700-3
    SSG: 15,3
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  • 4
    Online Resource
    Online Resource
    The additional PRC2 subunit and Sin3 histone deacetylase complex are required for the normal distribution of H3K27me3 occupancy and transcriptional silencing in Magnaporthe oryzae
    Wiley ; 2022
    In:  New Phytologist Vol. 236, No. 2 ( 2022-10), p. 576-589
    Details
    In: New Phytologist, Wiley, Vol. 236, No. 2 ( 2022-10), p. 576-589
    Abstract: Development in higher organisms requires proper gene silencing, partially achieved through trimethylation of lysine 27 on histone H3 (H3K27me3). However, how the normal distribution of this modification is established and maintained and how it affects gene expression remains unclear, especially in fungi. Polycomb repressive complex 2 (PRC2) catalyses H3K27me3 to assemble transcriptionally repressed facultative heterochromatin and is crucial in animals, plants, and fungi. Here, we report on the critical role of an additional PRC2 subunit in the normal distribution of H3K27me3 occupancy and the stable maintenance of gene repression in the rice fungal pathogen Magnaporthe oryzae . P55, identified as an additional PRC2 subunit, is physically associated with core subunits of PRC2 and is required for a complete level of H3K27me3 modification. Loss of P55 caused severe global defects in the normal distribution of H3K27me3 and transcriptional reprogramming on the H3K27me3‐occupied genes. Furthermore, we found that the Sin3 histone deacetylase complex was required to sustain H3K27me3 occupancy and stably maintain gene repression by directly interacting with P55. Our results revealed a novel mechanism by which P55 and Sin3 participate in the normal distribution of facultative heterochromatic modifications and the stable maintenance of gene repression in eukaryotes.
    Type of Medium: Online Resource
    ISSN: 0028-646X , 1469-8137
    URL: Issue
    URL: Article
    DOI: 10.1111/nph.v236.2
    DOI: 10.1111/nph.18383
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 208885-X
    detail.hit.zdb_id: 1472194-6
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  • 5
    Online Resource
    Online Resource
    〈p〉Long Intergenic Non-Coding RNA 01121 Promotes Breast Cancer Cell Proliferation, Migration, and Invasion via the 〈em〉miR-150-5p〈/em〉/HMGA2 Axis〈/p〉
    Informa UK Limited ; 2019
    In:  Cancer Management and Research Vol. Volume 11 ( 2019-12), p. 10859-10870
    Details
    In: Cancer Management and Research, Informa UK Limited, Vol. Volume 11 ( 2019-12), p. 10859-10870
    Type of Medium: Online Resource
    ISSN: 1179-1322
    URL: Journal
    URL: Article
    DOI: 10.2147/CMAR
    DOI: 10.2147/CMAR.S230367
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 2019
    detail.hit.zdb_id: 2508013-1
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  • 6
    Online Resource
    Online Resource
    Table_1.docx
    Frontiers Media SA ; 2022
    In:  Frontiers in Plant Science Vol. 13 ( 2022-4-7)
    Details
    In: Frontiers in Plant Science, Frontiers Media SA, Vol. 13 ( 2022-4-7)
    Abstract: The culprit of rice blast, Magnaporthe oryzae , is a filamentous fungus that seriously affects the yield and quality of rice worldwide. MoIst1, a subunit of ESCRT-III, is involved in identified ubiquitinated proteins and transports them into the intraluminal vesicles of multivesicular bodies (MVBs) for degradation in lysosomes. Here, we identify and characterize MoIst1 in M. oryzae . Disruption of MoIst1 leads to a significant decrease in sporulation and formation of appressoria, defects in response to oxidative stress, cell wall stress, hyperosmotic stress, and reduced pathogenicity. Deletion of MoIst1 also caused the decreased Pmk1 phosphorylation levels, appressorium formation, the delayed translocation and degradation of lipid droplets and glycogen, resulting in a decreased appressorium turgor. In addition, deletion of MoIst1 leads to an abnormal autophagy. In summary, our results indicate that MoIst1 is involved in sporulation, appressorium development, plant penetration, pathogenicity, and autophagy in M. oryzae .
    Type of Medium: Online Resource
    ISSN: 1664-462X
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fpls.2022.845139
    DOI: 10.3389/fpls.2022.845139.s001
    DOI: 10.3389/fpls.2022.845139.s002
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2687947-5
    detail.hit.zdb_id: 2613694-6
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  • 7
    Online Resource
    Online Resource
    Transcriptional Regulation of Autophagy-Related Genes by Sin3 Negatively Modulates Autophagy in Magnaporthe oryzae
    American Society for Microbiology ; 2023
    In:  Microbiology Spectrum Vol. 11, No. 3 ( 2023-06-15)
    Details
    In: Microbiology Spectrum, American Society for Microbiology, Vol. 11, No. 3 ( 2023-06-15)
    Abstract: Autophagy is a conserved degradation and recycling pathway in eukaryotes and is important for their normal growth and development. An appropriate status of autophagy is crucial for organisms which is tightly regulated both temporally and continuously. Transcriptional regulation of autophagy-related genes ( ATGs ) is an important layer in autophagy regulation. However, the transcriptional regulators and their mechanisms are still unclear, especially in fungal pathogens. Here, we identified Sin3, a component of the histone deacetylase complex, as a transcriptional repressor of ATGs and negative regulator of autophagy induction in the rice fungal pathogen Magnaporthe oryzae . A loss of SIN3 resulted in upregulated expression of ATGs and promoted autophagy with an increased number of autophagosomes under normal growth conditions. Furthermore, we found that Sin3 negatively regulated the transcription of ATG1 , ATG13 , and ATG17 through direct occupancy and changed levels of histone acetylation. Under nutrient-deficient conditions, the transcription of SIN3 was downregulated, and the reduced occupancy of Sin3 from those ATGs resulted in histone hyperacetylation and activated their transcription and in turn promoted autophagy. Thus, our study uncovers a new mechanism of Sin3 in modulating autophagy through transcriptional regulation. IMPORTANCE Autophagy is an evolutionarily conserved metabolic process and is required for the growth and pathogenicity of phytopathogenic fungi. The transcriptional regulators and precise mechanisms of regulating autophagy, as well as whether the induction or repression of ATGs is associated with autophagy level, are still poorly understood in M. oryzae . In this study, we revealed that Sin3 acts as a transcriptional repressor of ATGs to negatively regulate autophagy level in M. oryzae . Under the nutrient-rich conditions, Sin3 inhibits autophagy with a basal level through directly repressing the transcription of ATG1-ATG13-ATG17 . Upon nutrient-deficient treatment, the transcriptional level of SIN3 would decrease and dissociation of Sin3 from those ATG s associates with histone hyperacetylation and activates their transcriptional expression and in turn contributes to autophagy induction. Our findings are important as we uncover a new mechanism of Sin3 for the first time to negatively modulate autophagy at the transcriptional level in M. oryzae .
    Type of Medium: Online Resource
    ISSN: 2165-0497
    URL: Article
    DOI: 10.1128/spectrum.00171-23
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2023
    detail.hit.zdb_id: 2807133-5
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  • 8
    Online Resource
    Online Resource
    Inhibitory Effect and Mechanism of Trichoderma taxi and Its Metabolite on Trichophyton mentagrophyte
    MDPI AG ; 2022
    In:  Journal of Fungi Vol. 8, No. 10 ( 2022-09-25), p. 1006-
    Details
    In: Journal of Fungi, MDPI AG, Vol. 8, No. 10 ( 2022-09-25), p. 1006-
    Abstract: Trichophyton mentagrophytes is an important zoonotic dermatophyte, which seriously harms the skin of humans and animals. Chemical drugs are generally used for the prevention and treatment of the disease caused by T. mentagrophytes. Discovering new compounds from natural products is an important approach for new drug development. Trichoderma includes a variety of fungal species used for biological control of phytopathogenic fungi. However, the antifungal effects of Trichoderma and their metabolites on zoonotic fungal pathogens are largely unknown. Here, the effect of trichodermin, a metabolite derived from the plant endophytic fungus Trichoderma taxi, on T. mentagrophytes was examined, and the underlying mechanism was explored. T. mentagrophytes growth was suppressed significantly by trichodermin and completely inhibited under 1000 μg/mL trichodermin. The production and germination of T. mentagrophytes spores were remarkably reduced upon exposure to trichodermin, in comparison with control samples. Treatment of lesions caused by T. mentagrophytes on the rabbit skin with 1 mg/mL trichodermin prompted the healing process significantly; however, 20 mg/mL trichodermin was likely toxic to the skin. Under trichodermin treatment, the number of mitochondria in T. mentagrophytes increased significantly, while a few mitochondria-related genes decreased, indicating possible mitochondrial damage. In transcriptome analysis, the GO terms enriched by DEGs in the trichodermin-treated group included carbohydrate metabolic process, integral component of membrane, intrinsic component of membrane, and carbohydrate binding, while the enriched KEGG pathways comprised biosynthesis of secondary metabolites, glycolysis/gluconeogenesis, and carbon metabolism. By comparing the wild type and a gene deletion strain of T. mentagrophytes, we found that CDR1, an ABC transporter encoding gene, was involved in T. mentagrophytes sensitivity to trichodermin.
    Type of Medium: Online Resource
    ISSN: 2309-608X
    URL: Article
    DOI: 10.3390/jof8101006
    Language: English
    Publisher: MDPI AG
    Publication Date: 2022
    detail.hit.zdb_id: 2784229-0
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  • 9
    Online Resource
    Online Resource
    Table_2.docx
    Frontiers Media SA ; 2023
    In:  Frontiers in Plant Science Vol. 13 ( 2023-1-9)
    Details
    In: Frontiers in Plant Science, Frontiers Media SA, Vol. 13 ( 2023-1-9)
    Abstract: The endoplasmic reticulum (ER) acts as the starting point of the secretory pathway, where approximately one-third of the proteins are correctly folded and modified, loaded into vesicles, and transported to the Golgi for further processing and modification. In this process, COPII vesicles are responsible for transporting cargo proteins from the ER to the Golgi. Here, we identified the inner shell subunit of COPII vesicles (MoSec24B) and explored the importance of MoSec24B in the rice blast fungus. The targeted disruption of MoSec24B led to decreased growth, reduced conidiation, restricted glycogen and lipids utilization, sensitivity to the cell wall and hypertonic stress, the failure of septin-mediated repolarization of appressorium, impaired appressorium turgor pressure, and decreased ability to infect, which resulted in reduced pathogenicity to the host plant. Furthermore, MoSec24B functions in the three mitogen-activated protein kinase (MAPK) signaling pathways by acting with MoMst50. Deletion of MoSec24B caused reduced lipidation of MoAtg8, accelerated degradation of exogenously introduced GFP-MoAtg8, and increased lipidation of MoAtg8 upon treatment with a late inhibitor of autophagy (BafA1), suggesting that MoSec24B regulates the fusion of late autophagosomes with vacuoles. Together, these results suggest that MoSec24B exerts a significant role in fungal development, the pathogenesis of filamentous fungi and autophagy.
    Type of Medium: Online Resource
    ISSN: 1664-462X
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fpls.2022.1074107
    DOI: 10.3389/fpls.2022.1074107.s001
    DOI: 10.3389/fpls.2022.1074107.s002
    DOI: 10.3389/fpls.2022.1074107.s003
    DOI: 10.3389/fpls.2022.1074107.s004
    DOI: 10.3389/fpls.2022.1074107.s005
    DOI: 10.3389/fpls.2022.1074107.s006
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2687947-5
    detail.hit.zdb_id: 2613694-6
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  • 10
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    Online Resource
    The Amino Acid Permease MoGap1 Regulates TOR Activity and Autophagy in Magnaporthe oryzae
    MDPI AG ; 2022
    In:  International Journal of Molecular Sciences Vol. 23, No. 21 ( 2022-11-07), p. 13663-
    Details
    In: International Journal of Molecular Sciences, MDPI AG, Vol. 23, No. 21 ( 2022-11-07), p. 13663-
    Abstract: Rice is an important food crop all over the world. It can be infected by the rice blast fungus Magnaporthe oryzae, which results in a significant reduction in rice yield. The infection mechanism of M. oryzae has been an academic focus for a long time. It has been found that G protein, AMPK, cAMP-PKA, and MPS1-MAPK pathways play different roles in the infection process. Recently, the function of TOR signaling in regulating cell growth and autophagy by receiving nutritional signals generated by plant pathogenic fungi has been demonstrated, but its regulatory mechanism in response to the nutritional signals remains unclear. In this study, a yeast amino acid permease homologue MoGap1 was identified and a knockout mutant of MoGap1 was successfully obtained. Through a phenotypic analysis, a stress analysis, autophagy flux detection, and a TOR activity analysis, we found that the deletion of MoGap1 led to a sporulation reduction as well as increased sensitivity to cell wall stress and carbon source stress in M. oryzae. The ΔMogap1 mutant showed high sensitivity to the TOR inhibitor rapamycin. A Western blot analysis further confirmed that the TOR activity significantly decreased, which improved the level of autophagy. The results suggested that MoGap1, as an upstream regulator of TOR signaling, regulated autophagy and responded to adversities such as cell wall stress by regulating the TOR activity.
    Type of Medium: Online Resource
    ISSN: 1422-0067
    URL: Article
    DOI: 10.3390/ijms232113663
    Language: English
    Publisher: MDPI AG
    Publication Date: 2022
    detail.hit.zdb_id: 2019364-6
    SSG: 12
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