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- 저자 : Li Zegeng (검색결과 2 건)
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Wang Jieqiong,Li Zegeng,Zheng Lili,Tong Jiabing,Wang Chuanbo 한국응용생명화학회 2023 Applied Biological Chemistry (Appl Biol Chem) Vol.66 No.-
Circular RNAs (circRNAs) have been reported to be related to the initiation and progression of chronic obstructive pulmonary disease (COPD) by affecting the function of human bronchial epithelial cells (HBECs). Here, we aimed to investigate the function and mechanism of circ_0006872 in regulating COPD process using cigarette smoke extract (CSE)-induced 16HBEC in vitro. The results showed that circ_0006872 was increased in smokers without or with COPD, especially in smokers with COPD. Also, its expression was dose-dependently up-regulated by CSE exposure in 16HBECs. Functionally, circ_0006872 knockdown dramatically attenuated CSE-evoked proliferation arrest, apoptosis, inflammatory response and oxidative stress in 16HBECs. Mechanistically, circ_0006872/miR-485-3p/cyclin-dependent kinase inhibitor 1B (CDKN1B) formed a competitive endogenous RNA (ceRNA) network. CDKN1B was increased and miR-485-3p was decreased in COPD patients and CSE-induced 16HBECs. MiR-485-3p overexpression or CDKN1B knockdown protected 16HBEC against CSE-induced 16HBEC injury mentioned above. Moreover, rescue experiments showed that circ_0006872 regulated CSE-induced 16HBEC injury via miR-485-3p/CDKN1B axis. Circ_0006872 silencing protected against CSE-induced bronchial epithelial cell injury via miR-485-3p/CDKN1B axis, suggesting the potential application of circ_0006872 in preventing cigarette smoke-induced COPD.
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Jie Wu,Xueqi Wang,Zhaomin Yao,Qingqing Wu,Wei Fang,Zegeng Li,Dianlei Wang 대한약학회 2019 Archives of Pharmacal Research Vol.42 No.11
In the present study, the roles of AITC in upregulatingthe MRP1 expression and its relationship with theactivation of the Notch1 signaling pathway were investigatedby combining the in vivo and in vitro experiments. AITCwas administered to the COPD model rats and normal ratsto explore the association between Notch1 and MRP1. Thehuman bronchial epithelial cells were treated with DAPT,the Notch1 signaling pathway inhibitor, to verify the effectof Notch1 on the expression of AITC-induced MRP1. Comparedwith the control group, the expressions of Notch1,Hes1 (the target gene of Notch1) and MRP1 in the lung tissueof the COPD model group were significantly inhibited. In contrast to the COPD model group, the expressions ofMRP1, Hes1 and Notch1 dramatically up-regulated followingthe treatment with Low/High doses of AITC. The expressionof MRP1 in the 16 HBE cells was down-regulated bythe inhibition of Notch in a DAPT concentration-dependentmanner. Additionally, the AITC-induced up-regulation ofthe MRP1 expression was markedly impaired following the inhibition of Notch1. The above results indicated that thepulmonary function and the expression of MRP1 in COPDrats could be improved by AITC, which was partly dependenton the Notch1 signaling pathway. Therefore, targetingthe Notch signaling pathway may present as an effectivetherapeutic strategy for COPD treatment.
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