Rui Jiang^1,3,*, 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

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 mutations… More >

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 NOTCH3. Its expression was downregulated… More >

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 thickness (MT%). The… More >