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Data underlying the publication: Activation of PAR-2/p-ERK/GPX4 axis is involved in MCT-induced PAH and hypoxia-induced PASMCs proliferation

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4TU.ResearchData2024-10-10 更新2026-04-23 收录
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Title of the dataset: Data underlying the publication: Activation of PAR-2/p-ERK/GPX4 axis is involved in MCT-induced PAH and hypoxia-induced PASMCs proliferation. The dataset contains 5 pictures and 37 files in pzfx format. The 37 files in pzfx format contain experimental data related to the content of the pictures. For example, "Fig1A. media to vessel diameter ratio.pzfx" contains the data of "media to vessel diameter ratio" shown in A in Fig 1. There are a total of 5 pictures: Fig 1: Formation of MCT-induced rats PAH. Fig 2: An increase in the expression of protein PAR-2, p-ERK and GPX4 was observed in the lung tissue of rats with MCT-induced PAH. Fig 3: Hypoxia induces a time-dependent proliferation of PASMCs within 6 hours, accompanied by increased expression of PAR-2, p-ERK and GPX4. Fig 4: FSLL, a PAR-2 inhibitor, inhibited hypoxia-induced proliferation and regulated the expression of PAR-2, p-ERK and GPX4 in rat PASMCs. Fig5: Inhibition of MEK1/2/p-ERK with U0126 suppressed hypoxia-induced proliferation in rat PASMCs and regulated the expression of PAR -2 ,p - ERK,and GPX4. The research objectives are MCT-induced PAH rats and PASMCs. The type of research is an experimental prospective study. Methodology for data collection and type: All data collected were from animal and cells experiments, with all data types being numerical.

数据集题名:支撑该发表论文的数据集:蛋白酶激活受体2(PAR-2)/磷酸化细胞外调节蛋白激酶(p-ERK)/谷胱甘肽过氧化物酶4(GPX4)轴激活参与野百合碱(MCT)诱导的肺动脉高压(PAH)及缺氧诱导的肺动脉平滑肌细胞(PASMCs)增殖。本数据集包含5张图片及37份pzfx格式文件。该37份pzfx格式文件存储与上述图片配套的实验数据,例如"Fig1A. media to vessel diameter ratio.pzfx"包含图1A中展示的"血管中层直径与管径比值"对应实验数据。本次数据集共包含5张图片,分别为:图1:野百合碱(MCT)诱导的大鼠肺动脉高压(PAH)造模;图2:野百合碱(MCT)诱导肺动脉高压(PAH)大鼠的肺组织中,PAR-2、p-ERK及GPX4的蛋白表达水平显著升高;图3:缺氧可在6小时内以时间依赖性方式诱导肺动脉平滑肌细胞(PASMCs)增殖,同时伴随PAR-2、p-ERK及GPX4的表达上调;图4:PAR-2抑制剂FSLL可抑制缺氧诱导的大鼠肺动脉平滑肌细胞(PASMCs)增殖,并调控PAR-2、p-ERK及GPX4的表达水平;图5:使用U0126抑制MEK1/2/p-ERK通路,可缓解缺氧诱导的大鼠肺动脉平滑肌细胞(PASMCs)增殖,并调控PAR-2、p-ERK及GPX4的表达水平。本研究的研究对象为野百合碱(MCT)诱导的肺动脉高压(PAH)大鼠及肺动脉平滑肌细胞(PASMCs)。本研究类型为前瞻性实验研究。数据收集方法与数据类型:所有数据均来自动物实验与细胞实验,数据类型均为数值型数据。
创建时间:
2024-10-10
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