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  • Open Access

    ARTICLE

    NOTCH3 Mutations and CADASIL Phenotype in Pulmonary Arterial Hypertension Associated with Congenital Heart Disease

    Rui Jiang1,3,*, Kaisheng Lai2, Jianping Xu1, Xiang Feng1, Shaoye Wang1, Xiaojian Wang3, Zhe Liu2

    Congenital Heart Disease, Vol.17, No.6, pp. 675-686, 2022, DOI:10.32604/chd.2022.021626 - 11 October 2022

    Abstract Background: The etiology of pulmonary arterial hypertension associated with congenital heart disease (PAHCHD) is complicated and the phenotype is heterogeneous. Genetic defects of NOTCH3 were associated with cerebral disease and pulmonary hypertension. However, the relationship between NOTCH3 mutations and the clinical phenotype has not been reported in CHD-PAH. Methods: We eventually enrolled 142 PAH-CHD patients from Fuwai Hospital. Whole exome sequencing (WES) was performed to screen the rare deleterious variants of NOTCH3 gene. Results: This PAH-CHD cohort included 43 (30.3%) men and 99 (69.7%) women with the mean age 29.8 ± 10.9 years old. The pathogenic or likely pathogenic… More >

  • Open Access

    ARTICLE

    NOTCH3 Overexpression and Posttranscriptional Regulation by miR-150 Were Associated With EGFR–TKI Resistance in Lung Adenocarcinoma

    Youwei Zhang*, Bi Chen, Yongsheng Wang, Qi Zhao, Weijun Wu§, Peiying Zhang*, Liyun Miao, Sanyuan Sun*

    Oncology Research, Vol.27, No.7, pp. 751-761, 2019, DOI:10.3727/096504018X15372657298381

    Abstract Acquired resistance remains a key challenge in epidermal growth factor receptor (EGFR)–tyrosine kinase inhibitors (TKIs) therapy in lung adenocarcinoma (LUAD). Recent studies have shown that Notch signaling is associated with drug resistance. However, its role and possible mechanisms in EGFR-TKI resistance are not yet clear. In our study, we found that among four members of NOTCH1–4, only NOTCH3 was upregulated in LUAD tissues and TKI-resistant cell line (HCC827GR6). Knockdown of NOTCH3 by siRNA significantly inhibited proliferative ability, and decreased colony and sphere formation in HCC827GR6 cells. Then miR-150 was identified as a posttranscriptional regulator of… More >

  • Open Access

    ARTICLE

    Exploration of the Notch3‐HES5 signal pathway in monocrotaline‐induced pulmonary hypertension using rat model

    Xing Chen, Wu Zhou, Qinghua Hu, Lingjin Huang

    Congenital Heart Disease, Vol.14, No.3, pp. 396-402, 2019, DOI:10.1111/chd.12733

    Abstract Objective: This study explores the role of the Notch3‐HES5 signal pathway in mono‐ crotaline‐induced pulmonary hypertension (PH) using rat models.
    Method: Sprague Dawley rats (n = 45) were randomly grouped into normal group, control group, and model group. Rats in the model group were used to establish the PH rat model. Four weeks after model establishment, right catheterization was used to measure the mean pulmonary arterial pressure (mPAP) and right ventricular sys‐ tolic pressure (RVSP) to analyze hemodynamic changes. The severity of PH was as‐ sessed by the right ventricular hypertrophy index (RVHI) and percentage of media… More >

  • Open Access

    ARTICLE

    Astragaloside IV Enhances Cisplatin Chemosensitivity in Human Colorectal Cancer via Regulating NOTCH3

    Tao Xie*, Yao Li, Shi-Lei Li*, Hai-Feng Luo

    Oncology Research, Vol.24, No.6, pp. 447-453, 2016, DOI:10.3727/096504016X14685034103590

    Abstract Although astragaloside IV exhibits anti-inflammation, immunoregulatory, and anticancer properties, the chemosensitization effects of astragaloside IV in colorectal cancer have never been reported. Our study tested whether astragaloside could increase cisplatin sensitivity in colorectal cancer. CCK-8 assay was used to measure the cell viability of colorectal cancer cells. Quantitative real-time PCR and Western blot were performed to determine the mRNA and protein expression, respectively. Our data revealed that astragaloside IV administration significantly suppressed the cell growth of colorectal cancer cells, whereas no obvious cytotoxicity of astragaloside IV was observed in nonmalignant colonic cells. In addition, combined… More >

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