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  • Hindawi Limited  (5)
  • 1
    Online Resource
    Online Resource
    Tongxinluo Attenuates Myocardiac Fibrosis after Acute Myocardial Infarction in Rats via Inhibition of Endothelial-to-Mesenchymal Transition
    Hindawi Limited ; 2019
    In:  BioMed Research International Vol. 2019 ( 2019-06-16), p. 1-13
    Details
    In: BioMed Research International, Hindawi Limited, Vol. 2019 ( 2019-06-16), p. 1-13
    Abstract: Endothelial-to-mesenchymal transition (EndMT) is an essential mechanism in myocardial fibrosis (MF). Tongxinluo (TXL) has been confirmed to protect the endothelium against reperfusion injury after acute myocardial infarction (AMI). However, whether TXL can inhibit MF after AMI via inhibiting EndMT remained unknown. This study aims to identify the role of EndMT in MF after AMI as well as the protective effects and underlying mechanisms of TXL on MF. The AMI model was established in rats by ligating left anterior descending coronary artery. Then, rats were administered with high- (0.8 g·kg −1 ·d −1 ), mid- (0.4 g·kg −1 ·d −1 ), and low- (0.2 g·kg −1 ·d −1 ) dose Tongxinluo and benazepril for 4 weeks, respectively. Cardiac function, infarct size, MF, and related indicators of EndMT were measured. In vitro, human cardiac microvascular endothelial cells (HCMECs) were pretreated with TXL for 4 h and then incubated in hypoxia conditions for 3 days to induce EndMT. Under this hypoxic condition, neuregulin-1 (NRG-1) siRNA were further applied to silence NRG-1 expression. Immunofluorescence microscopy was used to assess expression of endothelial marker of vWF and fibrotic marker of Vimentin. Related factors of EndMT were determined by Western blot analysis. TXL treatment significantly improved cardiac function, ameliorated MF, reduced collagen of fibrosis area (types I and III collagen) and limited excessive extracellular matrix deposition (mmp2 and mmp9). In addition, TXL inhibited EndMT in cardiac tissue and hypoxia-induced HCMECs. In hypoxia-induced HCMECs, TXL increased the expression of endothelial markers, whereas decreasing the expression of fibrotic markers, partially through enhanced expressions of NRG-1, phosphorylation of ErbB2, ErbB4, AKT, and downregulated expressions of hypoxia inducible factor-1a and transcription factor snail. After NRG-1 knockdown, the protective effect of TXL on HCMEC was partially abolished. In conclusion, TXL attenuates MF after AMI by inhibiting EndMT and through activating the NRG-1/ErbB- PI3K/AKT signalling cascade.
    Type of Medium: Online Resource
    ISSN: 2314-6133 , 2314-6141
    URL: Article
    DOI: 10.1155/2019/6595437
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2019
    detail.hit.zdb_id: 2698540-8
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  • 2
    Online Resource
    Online Resource
    Andrographolide Inhibition of Th17-Regulated Cytokines and JAK1/STAT3 Signaling in OVA-Stimulated Asthma in Mice
    Hindawi Limited ; 2021
    In:  Evidence-Based Complementary and Alternative Medicine Vol. 2021 ( 2021-5-29), p. 1-11
    Details
    In: Evidence-Based Complementary and Alternative Medicine, Hindawi Limited, Vol. 2021 ( 2021-5-29), p. 1-11
    Abstract: Asthma has long been considered a disease of airway inflammation. The excessive or prolonged production of inflammatory mediators can result in airway remodeling and severe clinical syndromes such as dyspnea or even apnea. Therefore, pharmaceutical intervention is required to restrain the excessive release of such inflammatory mediators in control of asthma. Novel therapeutics and mechanistic insight are sought for the management of this chronic inflammatory disease. Andrographolide (AG) is a type of diterpenoid ester compound and is reported to demonstrate multiple properties such as antioxidation and anti-inflammation. However, the anti-inflammatory capacity of AG by regulating immunologic function in airway of asthma has not been fully studied to date. Therefore, this study investigates whether AG is capable of suppressing the inflammatory response of asthma in OVA-stimulated mice and the mechanism by which this is achieved. Animals were randomly divided into 4 groups: control group, OVA model group, OVA + AG (0.1 mg/ml) group, and OVA + dimethylsulfoxide (DMSO) group. The serum, BALF, and lung tissue of the mice were collected separately for the administration of ELISA, rt-PCR, western blot and pathological section and staining. We found that AG attenuated the OVA-induced production of IL-6, IL-17A, IL-17F, and RORγt; inhibited the OVA-mediated phosphorylation of JAK 1 and STAT3; and alleviated airway remodeling and the neutrophil infiltration of lung tissue. We conclude that AG inhibits the inflammatory response of asthma in OVA-stimulated mice by blocking the activation of Th17-regulated cytokines and the JAK1/STAT3 signaling pathway.
    Type of Medium: Online Resource
    ISSN: 1741-4288 , 1741-427X
    URL: Article
    DOI: 10.1155/2021/6862073
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2021
    detail.hit.zdb_id: 2148302-4
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  • 3
    Online Resource
    Online Resource
    Association of LAMA1 Single-Nucleotide Polymorphisms with Risk of Esophageal Squamous Cell Carcinoma among the Eastern Chinese Population
    Hindawi Limited ; 2023
    In:  Journal of Oncology Vol. 2023 ( 2023-2-14), p. 1-9
    Details
    In: Journal of Oncology, Hindawi Limited, Vol. 2023 ( 2023-2-14), p. 1-9
    Abstract: Introduction. LAMA1, also known as laminin subunit α1, is a member of the laminin family, which is widely reported to be a key basement membrane molecule that affects various biological activities and is associated with many kinds of diseases. We aimed to investigate the association between LAMA1single-nucleotide polymorphisms and the occurrence and progression of esophageal squamous cell carcinoma in the Chinese population. Method. 2,186 participants were collected retrospectively between October 2008 and January 2017, including 1,043 ESCC patients and 1,143 noncancer patients. A 2 mL blood sample was obtained intravenously for the LDR for SNP analysis. The 6 SNP loci of LAMA1 were selected and examined. We analyzed the association of several genetic models of 6 LAMA1 SNP loci, sex, age, smoking and drinking status, and the occurrence of esophageal squamous cell carcinoma. Results. In the rs62081531 G  〉  A locus, genotype GA was a protective factor for ESCC compared with GG (OR: 0.830, P = 0.046 ), especially among the younger and nondrinkers. At rs607230 T  〉  C, genotype TC was linked with a lower risk of ESCC compared with TT. (OR: 0.613, P = 0.034 ). Haplotype Frequencies revealed that Ars62081531Grs621993Ars539713Trs566655Ars73938538Crs607230 (OR: 0.803, P = 0.028 ) and Grs62081531Grs621993Ars539713Trs566655Crs73938538Crs607230 (OR: 0.679, P = 0.010 ) were strongly associated with lower susceptibility of ESCC. Conclusion. The LAMA1 rs62081531, rs539713, rs566655, and rs607230 polymorphisms were demonstrated to be related to susceptibility to ESCC in the Chinese population. LAMA1 SNPs may have a significant impact on the occurrence of esophageal cancer and may serve as potential diagnostic biomarkers.
    Type of Medium: Online Resource
    ISSN: 1687-8469 , 1687-8450
    URL: Article
    DOI: 10.1155/2023/6922909
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2023
    detail.hit.zdb_id: 2461349-6
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  • 4
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    Online Resource
    A Connexin-Based Biomarker Model Applicable for Prognosis and Immune Landscape Assessment in Lung Adenocarcinoma
    Hindawi Limited ; 2022
    In:  Journal of Oncology Vol. 2022 ( 2022-10-12), p. 1-12
    Details
    In: Journal of Oncology, Hindawi Limited, Vol. 2022 ( 2022-10-12), p. 1-12
    Abstract: Purpose. Gap junction protein (Connexin) family is the basic unit of cellular connection, whose multiple members were recently demonstrated to be associated with tumor progression. However, the expression pattern and prognostic value of connexin in lung adenocarcinoma (LUAD) have not yet been elucidated. Methods. Consensus cluster algorithm was first applied to determine a novel molecular subtype in LUAD based on connexin genes. The differentially expressed genes (DEGs) between two clusters were obtained to include in Cox regression analyses for the model construction. To examine the predictive capacity of the signature, survival curves and ROC plots were conducted. We implemented GSEA method to uncover the function effects enriched in the risk model. Moreover, the tumor immune microenvironment in LUAD was depicted by CIBERSORT and ssGSEA methods. Results. The integrated LUAD cohort (TCGA-LUAD and GSE68465) were clustered into two subtypes ( C 1 = 217 and C 2 = 296 ) based on 21 connexins and the clinical outcomes of LUAD cases in the two clusters showed remarkable discrepancy. Next, we collected 222 DEGs among two subclusters to build a prognostic model using stepwise Cox analyses. Our proposed model consisted of six genes that accurately forecast patient outcomes and differentiate patient risk. GSEA indicated that high-risk group was involved in tumor relevant pathways were activated in high-risk group, such as PI3K/AKT signaling, TGF-β pathway, and p53 pathway. Furthermore, LUAD cases with high-risk presented higher infiltration level of M2 macrophage and neutrophil, suggesting high-risk group were more likely to generate an immunosuppressive status. Conclusion. Our data identified a novel connexin-based subcluster in LUAD and further created a risk signature which plays a central part in prognosis assessment and clinical potency.
    Type of Medium: Online Resource
    ISSN: 1687-8469 , 1687-8450
    URL: Article
    DOI: 10.1155/2022/9261339
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2022
    detail.hit.zdb_id: 2461349-6
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  • 5
    Online Resource
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    Prokineticins as a Prognostic Biomarker for Low-Grade Gliomas: A Study Based on The Cancer Genome Atlas Data
    Hindawi Limited ; 2022
    In:  BioMed Research International Vol. 2022 ( 2022-7-7), p. 1-12
    Details
    In: BioMed Research International, Hindawi Limited, Vol. 2022 ( 2022-7-7), p. 1-12
    Abstract: Lower-grade glioma (LGG) is a crucial pathological type of glioma. Prokineticins have not been reported in LGG. Prokineticins as a member of the multifunctional chemokine-like peptide family are divided into two ligands: PROK1 and PROK2. We evaluated the role of PROK1 and PROK2 in LGG using TCGA database. We downloaded the datasets of LGG from TCGA and evaluated the influence of prokineticins on LGG survival by survival module. Correlations between clinical information and prokineticins expression were analyzed using logistic regression. Univariable survival and multivariate Cox analysis was used to compare several clinical characteristics with survival. Correlation between prokineticins and cancer immune infiltrates was explored using CIBERSORT and correlation module of GEPIA. We analyzed genes of PROK1 and PROK2 affecting LGG, screened differentially expressed genes (DEGs), interacted protein-protein with DEGs through the STRING website, then imported the results into the Cytospace software, and calculated the hub genes. To analyze whether hub genes and prokineticins are related, the relationship between PROK1 and PROK2 and hub genes was assessed and shown by heat map. In addition, gene set enrichment analysis (GSEA) was performed using the TCGA dataset. The univariate analysis using logistic regression and PROK1 and PROK2 showed opposite expression differences between tumor and normal tissues ( p 〈 0.05 ). PRO1 and PROK2 expressions showed significant differences in tumor grade, age, Iiscitrate DeHydrogenase (IDH) status, histological type, and 1P/19q codeletion. Multivariate analysis revealed that the up-regulated PROK1 and PROK2 expression is an independent prognostic factor for bad prognosis. Specifically, prokineticin expression level has significant correlations with infiltrating levels of Th1 cells, NK CD 56bright cells, and Mast cells in LGG. We screened 21 DEGs and obtained 5 hub genes (HOXC10, HOXD13, SOX4, GATA4, HOXA9). GSEA-identified FCMR activation, creation of C4 and C2 activators, and CD22-mediated BCR regulation in gene ontology (GO) were differentially enriched in high PROK1 and PROK2 expression phenotype pathway, cytoplasmic ribosomal proteins, and ribosome and were differentially enriched in the low PROK1 and PROK2 expression phenotype pathway. Prokineticins are a prognostic biomarker and the correlation between hub genes and LGG requires further attention.
    Type of Medium: Online Resource
    ISSN: 2314-6141 , 2314-6133
    URL: Article
    DOI: 10.1155/2022/2309339
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2022
    detail.hit.zdb_id: 2698540-8
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