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Targeting cathepsin L in the regulation of apoptosis in peripheral T-cell lymphoma 靶向组织蛋白酶L调控外周血t细胞淋巴瘤细胞凋亡的研究
4区 医学 Q4 TOXICOLOGY Pub Date : 2023-06-09 DOI: 10.1007/s13273-023-00359-w
Rui Zhang, Yanjie Ruan, Yiming Zhao, Fengbo Jin, Mingzhen Yang, Zhimin Zhai
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引用次数: 0
YTHDC1 inhibits cell proliferation and angiogenesis in cervical cancer by regulating m6A modification of SOCS4 mRNA YTHDC1通过调控m6A修饰SOCS4 mRNA抑制宫颈癌细胞增殖和血管生成
4区 医学 Q4 TOXICOLOGY Pub Date : 2023-05-30 DOI: 10.1007/s13273-023-00360-3
Sihe Chen, Yongheng Chen, Lanting Yu, Xiangmei Hu
{"title":"YTHDC1 inhibits cell proliferation and angiogenesis in cervical cancer by regulating m6A modification of SOCS4 mRNA","authors":"Sihe Chen, Yongheng Chen, Lanting Yu, Xiangmei Hu","doi":"10.1007/s13273-023-00360-3","DOIUrl":"https://doi.org/10.1007/s13273-023-00360-3","url":null,"abstract":"","PeriodicalId":18683,"journal":{"name":"Molecular & Cellular Toxicology","volume":"14 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135642738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
CircSLCO3A1 depletion ameliorates lipopolysaccharide-induced inflammation and apoptosis of human pulmonary alveolar epithelial cells through the miR-424-5p/HMGB3 pathway. CircSLCO3A1缺失通过miR-424-5p/HMGB3途径改善脂多糖诱导的人肺泡上皮细胞的炎症和凋亡。
IF 1.7 4区 医学 Q4 TOXICOLOGY Pub Date : 2023-05-25 DOI: 10.1007/s13273-023-00341-6
Yan Li, Chunmei Zhang, Zhongyan Zhao

Background: Recent studies have shown the pathogenesis of acute lung injury (ALI) involves circular RNA (circRNA). However, there are no data on the role of circSLCO3A1 in ALI and the underlying mechanism.

Objective: ALI-like cell injury was induced by stimulating human pulmonary alveolar epithelial cells (HPAEpiCs) using lipopolysaccharide (LPS). The expression of circSLCO3A1, miR-424-5p and high mobility group box 3 (HMGB3) was detected by quantitative real-time polymerase chain reaction. Cell viability and cell apoptosis were assessed by cell counting kit-8 (CCK-8) assay and flow cytometry analysis, respectively. Enzyme-linked immunosorbent assay was performed to determine the production of interleukin-1β (IL-1β), IL-6, tumor necrosis factor-α (TNF-α) and monocyte chemotactic protein 1 (MCP-1). Caspase-3 activity was detected by caspase-3 activity assay. Protein expression of inducible NOS (iNOS), cyclooxygenase-2 (COX2), p-p65 and p65 was analyzed by Western blot. The interactions among circSLCO3A1, miR-424-5p and HMGB3 were identified by dual-luciferase reporter assay, RNA immunoprecipitation assay and RNA pull-down assay.

Results: CircSLCO3A1 and HMGB3 expression were significantly increased, while miR-424-5p was decreased in LPS-treated HPAEpiCs and the serum of septic ALI patients in comparison with controls. CircSLCO3A1 knockdown assuaged LPS-induced HPAEpiC inflammation and apoptosis. Besides, circSLCO3A1 targeted miR-424-5p and regulated LPS-triggered HPAEpiC inflammation and apoptosis by binding to miR-424-5p. Under the treatment of LPS, miR-424-5p mediated HPAEpiC disorders by targeting HMGB3. Importantly, circSLCO3A1 modulated HMGB3 production by interacting with miR-424-5p.

Conclusion: CircSLCO3A1 absence assuaged LPS-induced HPAEpiC inflammation and apoptosis through the miR-424-5p/HMGB3 axis.

Highlights: CircSLCO3A1 expression was upregulated in LPS-induced HPAEpiCs and sepsis-induced ALI patients.CircSLCO3A1 depletion protected against LPS-induced HPAEpiC disorders.CircSLCO3A1 bound to miR-424-5p in HPAEpiCs.MiR-424-5p targeted HMGB3 in HPAEpiCs.CircSLCO3A1 regulated HMGB3 expression through miR-424-5p.

Supplementary information: The online version contains supplementary material available at 10.1007/s13273-023-00341-6.

背景:最近的研究表明,急性肺损伤(ALI)的发病机制涉及环状核糖核酸(circRNA)。然而,目前还没有关于circSLCO3A1在ALI中的作用及其潜在机制的数据。目的:用脂多糖(LPS)刺激人肺泡上皮细胞(HPAEpiCs),诱导ALI样细胞损伤。实时定量聚合酶链反应检测circSLCO3A1、miR-424-5p和高迁移率组盒3(HMGB3)的表达。细胞活力和细胞凋亡分别通过细胞计数试剂盒-8(CCK-8)测定和流式细胞术分析进行评估。采用酶联免疫吸附法测定白细胞介素-1β(IL-1β)、IL-6、肿瘤坏死因子-α(TNF-α)和单核细胞趋化蛋白1(MCP-1)的产生。Caspase-3活性测定法检测其活性。通过蛋白质印迹分析诱导型NOS(iNOS)、环氧合酶-2(COX2)、p-p65和p65的蛋白表达。通过双荧光素酶报告子分析、RNA免疫沉淀分析和RNA下拉分析鉴定了circSLCO3A1、miR-424-5p和HMGB3之间的相互作用。结果:与对照组相比,LPS处理的HPAEpiCs和脓毒症ALI患者血清中CircSLCO3A1和HMGB3的表达显著增加,而miR-424-5p的表达降低。CircSLCO3A1敲低可减轻LPS诱导的HPAEpiC炎症和细胞凋亡。此外,circSLCO3A1靶向miR-424-5p,并通过与miR-424-5p结合来调节LPS触发的HPAEpiC炎症和细胞凋亡。在LPS的治疗下,miR-424-5p通过靶向HMGB3介导HPAEpiC疾病。重要的是,circSLCO3A1通过与miR-424-5p相互作用调节HMGB3的产生。结论:circSLCO3A1的缺失通过miR-424-5p/HMGB3轴减轻了LPS诱导的HPAEpiC炎症和细胞凋亡。亮点:CircSLCO3A1在LPS诱导的HPAEpiCs和败血症诱导的ALI患者中表达上调。CircSLCO3A1耗竭对LPS诱导的HPAEpiC疾病具有保护作用。CircSLCO3A1与HPAEpiCs中的miR-424-5p结合。miR-424-5p靶向HPAEpiCs中的HMGB3。CircSLCO3A 1通过miR-424-5p.调节HMGB3的表达。补充信息:在线版本包含补充材料,可访问10.1007/s13273-023-00341-6。
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引用次数: 1
CircKLHL2 mitigates septic lung injury via circKLHL2-miR-338-3p-ATF6 ceRNA pathway CircKLHL2通过CircKLHL2 - mir -338-3p- atf6 ceRNA通路减轻脓毒性肺损伤
IF 1.7 4区 医学 Q4 TOXICOLOGY Pub Date : 2023-05-09 DOI: 10.1007/s13273-023-00349-y
Chunmei Zhang, Ruoran Wu, Zhongyan Zhao
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引用次数: 0
Premature ovarian insufficiency associated with environmental chemical exposure among Korean women: a study based on the Korean National Environmental Health Survey (2009–2012) 韩国女性过早卵巢功能不全与环境化学物质暴露相关:一项基于韩国国家环境健康调查的研究(2009-2012)
IF 1.7 4区 医学 Q4 TOXICOLOGY Pub Date : 2023-05-05 DOI: 10.1007/s13273-023-00358-x
YunJeong Kim, Eunha Oh, Min-kyung Shin, D. Nam, So-Young Jeon, J. Yu, J. Song, Dohsik Minn, Eunil Lee
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引用次数: 0
Low-dose-rate gamma radiation aggravates titanium dioxide nanoparticle-induced lung injury in mice 低剂量率γ辐射加重二氧化钛纳米粒子诱导的小鼠肺损伤
IF 1.7 4区 医学 Q4 TOXICOLOGY Pub Date : 2023-05-04 DOI: 10.1007/s13273-023-00353-2
Sohi Kang, Hae-June Lee, Y. Son, M. Bae, W. Jo, J. Park, Sohee Jeong, Changjong Moon, I. Shin, C. Lee, J. Kim
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引用次数: 0
FGD5-AS1 promotes growth and mobility of trophoblast cells by regulating IGF2 via sponging miR-16-5p in pre-eclampsia FGD5-AS1在子痫前期通过海绵化miR-16-5p调控IGF2,促进滋养细胞的生长和迁移
IF 1.7 4区 医学 Q4 TOXICOLOGY Pub Date : 2023-04-26 DOI: 10.1007/s13273-023-00357-y
Limei Quan, Yan Jin, Jianfang Wang, Xiwang Dai, Shuli Zhu, Zengwei Sheng
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引用次数: 0
Reduced cellular process and developmental process genotoxicity of polystyrene nanoplastics in zebrafish embryogenesis using Aurelia aurita proteins 聚苯乙烯纳米塑料在斑马鱼胚胎发生中的细胞过程和发育过程遗传毒性研究
IF 1.7 4区 医学 Q4 TOXICOLOGY Pub Date : 2023-04-20 DOI: 10.1007/s13273-023-00356-z
In Hae Park, Sun Woo Geum, Min-Kyeong Yeo
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引用次数: 0
The efficacy of Plantago asiatica L. water extract on lipid metabolism in a high-fat diet-induced obese C57BL/6 mice 车前草水提取物对高脂饮食诱导的肥胖C57BL/6小鼠脂质代谢的影响
IF 1.7 4区 医学 Q4 TOXICOLOGY Pub Date : 2023-04-20 DOI: 10.1007/s13273-023-00355-0
M. Jung, Soyoung Kim, Yujin Kim, Mi Ryeo Kim
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引用次数: 0
PCSK9 regulates myocardial ischemia–reperfusion injury through parkin/pink1-mediated autophagy pathway PCSK9通过parkin/pink1介导的自噬途径调节心肌缺血再灌注损伤
IF 1.7 4区 医学 Q4 TOXICOLOGY Pub Date : 2023-03-24 DOI: 10.1007/s13273-023-00352-3
Guan-fen Huang, Hailong Bao, Peng-fei Zhan, Xiyang Lu, Zonggang Duan, Xinlin Xiong, Muzhi Lin, Bing Wang, Hongxin An, Luanda Xiahou, Haiyan Zhou, Zhenhua Luo, Wei Li
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引用次数: 1
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Molecular & Cellular Toxicology
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