MicroRNA - 200c - 3p通过ANGII和ACE2/ANG1 - 7途径调控海水诱导的急性肺损伤

IF 2.4 4区 医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL
Minlong Zhang, Lixin Xie
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引用次数: 0

摘要

细胞凋亡是海水吸入性急性肺损伤(ALI)的主要特征。局部血管紧张素(ANG)系统血管紧张素转换酶(ACE)‑2/ANG1‑7/Mas轴和ANGII/血管紧张素II受体1型(AT1)在细胞凋亡中发挥重要作用。MicroRNA (miR)‑200c‑3p参与了ACE‑2通路的调控,但其在海水诱导ALI中的作用和机制尚不清楚。本研究建立海水- ALI肺组织和细胞模型,在miR - 200c - 3p下调后,采用western blotting检测凋亡相关蛋白ACE2、ANGII、ANG1 - 7。此外,通过反转录定量PCR检测miR - 200c - 3p。miR - 200c - 3p和ACE2之间的靶标关系通过双荧光素酶报告基因实验得到证实。海水刺激增加了miR - 200c - 3p、ANGII的表达,降低了ACE - 2/ANG1 - 7的表达,诱导了凋亡相关蛋白表达的变化。AT1阻断剂可抑制细胞凋亡,海水刺激后加入ANG1‑7可消除细胞凋亡。此外,miR - 200c - 3p抑制细胞凋亡,降低ANGII的表达,但增加ACE - 2/ANG1 - 7的表达。这些结果表明miR - 200c - 3p的表达增加是海水诱导ALI的重要原因,这种现象是通过抑制ACE2/ANG1 - 7途径实现的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
MicroRNA‑200c‑3p regulates seawater‑induced acute lung injury via ANGII and ACE2/ANG1‑7 pathways
Apoptosis is a main characteristic of seawater aspiration‑induced acute lung injury (ALI). The local angiotensin (ANG) system angiotensin converting enzyme (ACE)‑2/ANG1‑7/Mas axis and ANGII/angiotensin II receptor type 1 (AT1) play an important role in apoptosis. MicroRNA (miR)‑200c‑3p is involved in the regulation of the ACE‑2 pathway, but its role and mechanism in seawater‑induced ALI remain to be elucidated. In the present study, seawater‑ALI lung tissue and cell model was established and apoptosis‑related proteins, ACE2, ANGII, ANG1‑7 were detected by western blotting following downregulation of miR‑200c‑3p. In addition, miR‑200c‑3p was detected by reverse transcription‑quantitative PCR. The target relationship between miR‑200c‑3p and ACE2 was confirmed by dual‑luciferase reporter assay. Seawater stimulation increased the expression of miR‑200c‑3p, ANGII and decreased ACE‑2/ANG1‑7 expression and induced changes of apoptosis‑related protein expression. Apoptosis can be inhibited by AT1 blocker and abrogated by addition of ANG1‑7 following seawater stimulation. In addition, inhibition of miR‑200c‑3p suppressed apoptosis and decreased the expression of ANGII, but increased the ACE‑2/ANG1‑7 expression. These results suggested that increased expression of miR‑200c‑3p was an important cause in seawater‑induced ALI and this phenomenon was through inhibition of ACE2/ANG1‑7 pathway.
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来源期刊
Experimental and therapeutic medicine
Experimental and therapeutic medicine MEDICINE, RESEARCH & EXPERIMENTAL-
CiteScore
1.50
自引率
0.00%
发文量
570
审稿时长
1 months
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