LncRNA HOTAIR accelerates free fatty acid-induced inflammatory response in HepG2 cells by recruiting SRSF1 to stabilize MLXIPL mRNA

IF 2 4区生物学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY

Cytotechnology Pub Date : 2024-02-20 DOI:10.1007/s10616-023-00614-x

Bo Guo, Shengzhe Yan, Lei Zhai, Yanzhen Cheng

{"title":"LncRNA HOTAIR accelerates free fatty acid-induced inflammatory response in HepG2 cells by recruiting SRSF1 to stabilize MLXIPL mRNA","authors":"Bo Guo, Shengzhe Yan, Lei Zhai, Yanzhen Cheng","doi":"10.1007/s10616-023-00614-x","DOIUrl":null,"url":null,"abstract":"<p>LncRNA HOTAIR has been reported to be associated with metabolic diseases of the liver. However, the effect of HOTAIR on non-alcoholic fatty liver disease (NAFLD) inflammation and its potential mechanism have not been reported. Genes and proteins expression were detected by qRT-PCR and Western blot respectively. The level of inflammatory cytokines was assessed by ELISA. HepG2 cell viability was detected by MTT assay. TG level and lipid accumulation were measured by Assay Kit and Oil red O staining, respectively. Direct binding relationship between HOTAIR and Serine/arginine splicing factor 1 (SRSF1), SRSF1 and MLX interacting protein like (MLXIPL) were confirmed by RNA-pull down and RIP assay. HOTAIR was highly expressed in free fatty acids (FFA)-treated HepG2 cells. HOTAIR knockdown alleviated FFA-induced inflammation of HepG2 cells. Then further analysis showed that HOTAIR and SRSF1 had a mutual binding relationship, and HOTAIR maintained MLXIPL mRNA stability via recruiting SRSF1 in HepG2 cells. Moreover, the inhibitory effect of HOTAIR knockdown on FFA-induced inflammation in HepG2 cells was reversed by MLXIPL overexpression. HOTAIR accelerates inflammation of FFA-induced HepG2 cells by recruiting SRSF1 to stabilize MLXIPL mRNA, which will help to find new effective strategies for NAFLD therapy.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"30 1","pages":""},"PeriodicalIF":2.0000,"publicationDate":"2024-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cytotechnology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1007/s10616-023-00614-x","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOTECHNOLOGY & APPLIED MICROBIOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

LncRNA HOTAIR has been reported to be associated with metabolic diseases of the liver. However, the effect of HOTAIR on non-alcoholic fatty liver disease (NAFLD) inflammation and its potential mechanism have not been reported. Genes and proteins expression were detected by qRT-PCR and Western blot respectively. The level of inflammatory cytokines was assessed by ELISA. HepG2 cell viability was detected by MTT assay. TG level and lipid accumulation were measured by Assay Kit and Oil red O staining, respectively. Direct binding relationship between HOTAIR and Serine/arginine splicing factor 1 (SRSF1), SRSF1 and MLX interacting protein like (MLXIPL) were confirmed by RNA-pull down and RIP assay. HOTAIR was highly expressed in free fatty acids (FFA)-treated HepG2 cells. HOTAIR knockdown alleviated FFA-induced inflammation of HepG2 cells. Then further analysis showed that HOTAIR and SRSF1 had a mutual binding relationship, and HOTAIR maintained MLXIPL mRNA stability via recruiting SRSF1 in HepG2 cells. Moreover, the inhibitory effect of HOTAIR knockdown on FFA-induced inflammation in HepG2 cells was reversed by MLXIPL overexpression. HOTAIR accelerates inflammation of FFA-induced HepG2 cells by recruiting SRSF1 to stabilize MLXIPL mRNA, which will help to find new effective strategies for NAFLD therapy.

Abstract Image

查看原文本刊更多论文

LncRNA HOTAIR通过招募SRSF1稳定MLXIPL mRNA，加速游离脂肪酸诱导的HepG2细胞炎症反应

据报道，LncRNA HOTAIR与肝脏代谢疾病有关。然而，HOTAIR对非酒精性脂肪肝（NAFLD）炎症的影响及其潜在机制尚未见报道。基因和蛋白质表达分别通过 qRT-PCR 和 Western 印迹进行检测。炎症细胞因子的水平通过 ELISA 进行评估。MTT 试验检测了 HepG2 细胞的活力。TG水平和脂质积累分别通过检测试剂盒和油红O染色法进行检测。通过RNA牵引和RIP实验证实了HOTAIR与丝氨酸/精氨酸剪接因子1（SRSF1）、SRSF1和MLX相互作用蛋白（MLXIPL）之间的直接结合关系。HOTAIR 在游离脂肪酸（FFA）处理的 HepG2 细胞中高表达。敲除 HOTAIR 可减轻游离脂肪酸诱导的 HepG2 细胞炎症反应。进一步的分析表明，HOTAIR与SRSF1存在相互结合的关系，HOTAIR通过招募SRSF1维持HepG2细胞中MLXIPL mRNA的稳定性。此外，HOTAIR敲除对FFA诱导的HepG2细胞炎症的抑制作用被MLXIPL过表达逆转。HOTAIR通过招募SRSF1来稳定MLXIPL mRNA，从而加速了FFA诱导的HepG2细胞的炎症反应，这将有助于为非酒精性脂肪肝的治疗找到新的有效策略。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Cytotechnology 生物-生物工程与应用微生物

CiteScore

4.10

自引率

0.00%

发文量

审稿时长

6-12 weeks

期刊介绍： The scope of the Journal includes: 1. The derivation, genetic modification and characterization of cell lines, genetic and phenotypic regulation, control of cellular metabolism, cell physiology and biochemistry related to cell function, performance and expression of cell products. 2. Cell culture techniques, substrates, environmental requirements and optimization, cloning, hybridization and molecular biology, including genomic and proteomic tools. 3. Cell culture systems, processes, reactors, scale-up, and industrial production. Descriptions of the design or construction of equipment, media or quality control procedures, that are ancillary to cellular research. 4. The application of animal/human cells in research in the field of stem cell research including maintenance of stemness, differentiation, genetics, and senescence, cancer research, research in immunology, as well as applications in tissue engineering and gene therapy. 5. The use of cell cultures as a substrate for bioassays, biomedical applications and in particular as a replacement for animal models.