Archives of biochemistry and biophysics最新文献

{"title":"Corrigendum to \"Benzene induces myelodysplasia and hematotoxicity via ferroptosis induction and downregulation of GPX4\" [Arch. Biochem. Biophys. 773 (2025) 110606].","authors":"Renjun Bao, Ti Zhang, Yuhua Fu, Hongyun Song, Mian Wang, Huijing Hu, Yonghua Yao","doi":"10.1016/j.abb.2025.110621","DOIUrl":"https://doi.org/10.1016/j.abb.2025.110621","url":null,"abstract":"","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":" ","pages":"110621"},"PeriodicalIF":3.0,"publicationDate":"2025-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145124055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metformin attenuates placental oxidative stress through Nrf2/Keap1 signaling in preeclampsia rats","authors":"Miao Xu ,&nbsp;Xinhuan Zhang ,&nbsp;Huijing Ma ,&nbsp;Fang Wang ,&nbsp;Mengnan Li ,&nbsp;Ruidan Zhang ,&nbsp;Lijun Yang ,&nbsp;Nan Zhang ,&nbsp;Xiaorui Ren ,&nbsp;Huiniu Hao ,&nbsp;Zhuanghui Hao ,&nbsp;Hailan Yang","doi":"10.1016/j.abb.2025.110622","DOIUrl":"10.1016/j.abb.2025.110622","url":null,"abstract":"<div><h3>Background</h3><div>Preeclampsia (PE) represents a severe gestational disorder defined by the development of hypertension accompanied by systemic organ dysfunction during pregnancy, affecting 3 %–5 % of pregnancies globally and contributing markedly to maternal-perinatal mortality. Placental oxidative stress (OS) is a key pathophysiological driver. A well-known antidiabetic drug metformin (MET) possesses anti-inflammatory and antioxidant properties, suggesting its therapeutic potential for PE; however, its molecular mechanisms remain unclear.</div></div><div><h3>Methods</h3><div>A PE-like rat model was established using N(ω)-nitro-<span>l</span>-arginine methyl ester (<span>l</span>-NAME), a nitric oxide synthase inhibitor. Pregnant Sprague-Dawley rats (n = 30) were divided into the control, <span>l</span>-NAME, and <span>l</span>-NAME + MET groups. We evaluated clinical parameters (blood pressure, proteinuria, placental, and renal histopathology), angiogenic factors (soluble fms-like tyrosine kinase-1 (sFlt-1) and placental growth factor (PlGF)), and OS markers (malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT)). Nuclear factor erythroid 2-related factor 2 (Nrf2)/Kelch Like ECH Associated Protein 1 (Keap1) signaling analysis employed western blotting, immunohistochemistry, immunofluorescence and reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Molecular docking and dynamics simulations explored MET's interaction with the Nrf2-Keap1 complex.</div></div><div><h3>Results</h3><div>Significant reductions in systolic blood pressure, proteinuria, and placental-renal histopathological damage, along with improved fetal weight, were observed with MET treatment. It normalized the sFlt-1/PlGF ratio and boosted antioxidant enzyme activities. MET promoted nuclear Nrf2 translocation, upregulated NAD(P)H:quinone oxidoreductase 1 (NQO1), and suppressed Keap1. Molecular modeling suggests that MET-induced destabilization of the Nrf2-Keap1 complex facilitates Nrf2 dissociation.</div></div><div><h3>Conclusion</h3><div>MET mitigates <span>l</span>-NAME induced oxidative stress by activating the Nrf2 signaling pathway, highlighting its potential as a novel therapeutic target for PE management.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"774 ","pages":"Article 110622"},"PeriodicalIF":3.0,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145102499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Temperature and cosolute regulate the liquid-liquid phase separation in BSA solutions","authors":"Brigitte Merino Naranjo ,&nbsp;Erica Fuoco ,&nbsp;Rosa Bartucci ,&nbsp;Rita Guzzi","doi":"10.1016/j.abb.2025.110620","DOIUrl":"10.1016/j.abb.2025.110620","url":null,"abstract":"<div><div>Biomolecular condensates form <em>in vivo</em> in the crowded cellular environment and are favoured in macromolecules containing low structural complexity or large portions of disordered regions. The liquid-liquid phase separation (LLPS) of protein solutions, in which macromolecule-rich regions are separated from the aqueous solution, can also be observed <em>in vitro</em> under specific experimental conditions of temperature, pH, pressure and components concentration. In this study, we investigate the formation of LLPS of bovine serum albumin (BSA) induced by polyethylene glycol (PEG-5000) and temperature. The LLPS of BSA solutions and droplets formation were assessed and characterized by temperature dependent turbidity, optical microscopy and infrared spectroscopy experiments. The results show that the lower the PEG concentration, the lower the LLPS transition temperature of BSA solution. At PEG concentration of 10 % (w/v) the average diameter of BSA droplets is about 9 μm at 10 °C, decreases to about 3 μm at 20 °C and at higher temperature the droplets dissolve and a homogeneous phase is observed. The real time formation of the BSA droplets is also followed by ATR-FTIR kinetic experiments that allow an estimate of protein concentration in the droplets giving a value 50 times higher than the initial solution (100 μM). No variation of the protein secondary structure within the condensates compared to the homogeneous phase is evidenced.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"774 ","pages":"Article 110620"},"PeriodicalIF":3.0,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145091084","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA CTB-31O20.2 promotes the progression of hepatocellular carcinoma by targeting the miR-139-5p/ROCK1 axis","authors":"Dizhong Ye ,&nbsp;Biyan Chen ,&nbsp;Xiangfa Wang,&nbsp;Weiwei Chen,&nbsp;Feng Ye,&nbsp;Guangqian Quan","doi":"10.1016/j.abb.2025.110619","DOIUrl":"10.1016/j.abb.2025.110619","url":null,"abstract":"<div><div>Hepatocellular carcinoma (HCC) is a primary cause of mortality from cancer, necessitating novel insights into its molecular underpinnings. Recent evidence points to the significant roles of lncRNAs in HCC progression, among which CTB-31O20.2 has emerged as a potentially crucial player. This study utilized RNA sequencing to identify differentially expressed lncRNAs in HCC tissues, focusing on CTB-31O20.2. We employed RT-qPCR, Western blotting, and dual-luciferase reporter assays to evaluate the expression patterns of CTB-31O20.2 in HCC cells and its interactions with miR-139-5p and Rho-associated coiled-coil containing protein kinase1 (ROCK1). In vivo effects were analyzed using a xenograft mouse model. CTB-31O20.2 was significantly upregulated in HCC tissues and cell lines. Silencing CTB-31O20.2 in Hep3B and HepG2 cells reduced malignancy, evidenced by decreased viability, colony formation, and invasion, and increased apoptosis. These cellular behaviors were associated with alterations in apoptosis-related proteins and epithelial-mesenchymal transition (EMT) markers. CTB-31O20.2 was shown to interact with miR-139-5p, and its silencing upregulated miR-139-5p, leading to reduced ROCK1 expression. Conversely, miR-139-5p inhibition reversed the anti-tumor effects of CTB-31O20.2 silencing. Overexpression of ROCK1 negated the inhibitory effects on HCC cell malignancy induced by CTB-31O20.2 depletion. In vivo, CTB-31O20.2 silencing significantly reduced tumor growth in a xenograft model. Our findings reveal that CTB-31O20.2 contributes to HCC progression by modulating miR-139-5p and ROCK1 expression. These results highlight CTB-31O20.2 as a potential therapeutic target in HCC, providing a new perspective on the mechanisms driving HCC pathogenesis and progression.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"774 ","pages":"Article 110619"},"PeriodicalIF":3.0,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145079475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction notice to \"WNK1 phosphorylation sites in TBC1D1 and TBC1D4 modulate cell surface expression of GLUT1\" [Arch. Biochem. Biophys. 679 (2020) 108223].","authors":"Andreia F A Henriques, Paulo Matos, Ana Sofia Carvalho, Mikel Azkargorta, Felix Elortza, Rune Matthiesen, Peter Jordan","doi":"10.1016/j.abb.2025.110614","DOIUrl":"10.1016/j.abb.2025.110614","url":null,"abstract":"","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":" ","pages":"110614"},"PeriodicalIF":3.0,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145058326","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A kinetic and spectroscopic study of tetrahydrodipicolinate N-succinyltransferase (DapD) from Serratia marcescens and its inactivation by Cu2+","authors":"Benjamin Hayes ,&nbsp;Mason Zuelzke ,&nbsp;Abigail M. Smith ,&nbsp;Blake Edmonson ,&nbsp;David O. Osula ,&nbsp;Nicholas A. Clanton ,&nbsp;Halli Hollingsworth ,&nbsp;Lilian Chooback ,&nbsp;Molly Lockart ,&nbsp;Corey M. Johnson","doi":"10.1016/j.abb.2025.110607","DOIUrl":"10.1016/j.abb.2025.110607","url":null,"abstract":"<div><div>Tetrahydrodipicolinate <em>N</em>-succinyltransferase (DapD) catalyzes the reaction of tetrahydrodipicolinate (THDP) and succinyl-CoA to form (<em>S</em>)-2-(3-carboxypropanamido)-6-oxoheptanedioic acid and coenzyme A. The enzyme is in the diaminopimelate-lysine biosynthesis pathway which produces two metabolites necessary for the survival and growth of pathogenic bacteria. Since lysine is an essential amino acid to humans, DapD is a potentially safe target for antibiotic therapies. Despite its identification as an exploitable target, details regarding the mechanism of DapD and its inhibition remain poorly resolved. In this work, the DAPD gene from <em>Serratia marcescens</em> has been optimally expressed in <em>E. coli</em> host cells and purified. Initial velocity patterns generated using two assays (one direct and one coupled) are consistent with a rapid equilibrium ordered bi bi kinetic mechanism. Therefore, conversion of the central enzyme complexes (chemistry) is thought to be the rate-limiting step in the reaction. Data fitted to the appropriate rate equation provide estimates of kinetic constants for the reaction (K_ia (2-AP) = 1.9 ± 0.26 mM and K_b (succinyl-CoA) = 87 ± 15 μM). <em>Sm</em>DapD is rapidly and specifically inactivated in the presence of Cu²⁺ at low concentrations, yet activity was protected in a reducing environment (1 mM DTT). Correspondingly, the internal tryptophan fluorescence of DapD is quenched by Cu²⁺ with a K_D of 2.7 μM, and emission spectra are comparable to chemically denatured DapD. Fluorescence quenching was relieved in the presence of DTT or EDTA. EPR spectra are consistent with Cu²⁺ binding to enzymatic histidine and being reduced to Cu⁺. These data suggest Cu²⁺ binding to the enzyme as well as an oxidative inactivation that results in significant structural changes and denaturing. Together, the mechanistic detail and characterization of the Cu²⁺ inactivation will inform the targeting of DapD with new antibiotic therapies.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"774 ","pages":"Article 110607"},"PeriodicalIF":3.0,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145032654","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Benzene induces myelodysplasia and hematotoxicity via ferroptosis induction and downregulation of GPX4","authors":"Renjun Bao ,&nbsp;Ti Zhang ,&nbsp;Yuhua Fu ,&nbsp;Hongyun Song ,&nbsp;Mian Wang ,&nbsp;Huijing Hu ,&nbsp;Yonghua Yao","doi":"10.1016/j.abb.2025.110606","DOIUrl":"10.1016/j.abb.2025.110606","url":null,"abstract":"<div><h3>Background</h3><div>Benzene, a ubiquitous industrial chemical, is a well-established environmental toxin associated with hematological disorders such as myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML), which are characterized by impaired hematopoiesis and bone marrow failure. This study investigates the role of ferroptosis, an iron-dependent form of cell death, in benzene-induced hematotoxicity, focusing on the repression of glutathione peroxidase 4 (GPX4), a critical regulator of ferroptosis.</div></div><div><h3>Materials and methods</h3><div>Male C57BL/6 mice were exposed to benzene at various doses over six weeks. Ferroptosis markers, oxidative stress levels, and GPX4 expression were assessed in bone marrow and CD34⁺ hematopoietic stem cells using biochemical assays, PCR, and Western blotting. Ferroptosis was induced <em>via</em> CRISPR-Cas9-mediated GPX4 knockout and the ferroptosis inducer erastin. The protective effects of ferroptosis inhibitors (DFO and Fer-1) were also evaluated.</div></div><div><h3>Results</h3><div>Benzene exposure led to a dose-dependent reduction in red and white blood cell counts, hemoglobin levels, and bone marrow cellularity. It also elevated oxidative stress markers, disrupted iron metabolism, and suppressed GPX4 expression. GPX4 knockout and erastin treatment mimicked benzene-induced effects, causing decreased cell viability, impaired colony formation, and lipid peroxidation accumulation. Administration of ferroptosis inhibitors reversed these effects, restoring cellular function, reducing reactive oxygen species (ROS), and preventing oxidative damage. GPX4 overexpression further protected against benzene-induced ferroptosis and hematopoietic toxicity.</div></div><div><h3>Conclusion</h3><div>Ferroptosis plays a central role in benzene-induced hematotoxicity, mediated by oxidative stress, disruption of iron metabolism, and suppression of GPX4. Ferroptosis inhibitors show potential as therapeutic agents for mitigating benzene-induced hematological damage, offering novel therapeutic strategies for disorders induced by environmental toxins.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"773 ","pages":"Article 110606"},"PeriodicalIF":3.0,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145008025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hydrogen sulfide (H2S) alleviates diabetic myocardial fibrosis by suppressing pyroptosis via inhibiting DNMT3a-mediated Sestrin2 CpG promoter hypermethylation","authors":"Yi Liu ,&nbsp;Ting Yang ,&nbsp;Hongming Hu ,&nbsp;Qi Yang ,&nbsp;Jun Yang ,&nbsp;Chun Chu","doi":"10.1016/j.abb.2025.110605","DOIUrl":"10.1016/j.abb.2025.110605","url":null,"abstract":"<div><h3>Background</h3><div>Diabetic cardiomyopathy (DCM) represents an important concern associated with diabetes, inhibiting pyroptosis has shown promising results in alleviating DCM symptoms. The objective of this work is to investigate the role and underlying mechanism of hydrogen sulfide (H₂S) in the suppression of pyroptosis in the context of diabetic myocardial fibrosis (MF).</div></div><div><h3>Methods</h3><div>The effect of H₂S on pyroptosis was detected using CCK-8, ELISA, and flow cytometry. The expression of Sestrin2 and its DNA methylation modification, as well as the quantification of pyroptosis-related proteins and the activation of the TLR4/MyD88/NF-κB signaling pathway, were measured using Western blot, ChIP, Immunofluorescence, and methylation-specific quantitative PCR. To establish a type 2 diabetes rat model, a high-fat diet was administered, followed by injection of streptozotocin (HFD/STZ). After five weeks, the rats received H₂S treatment for four weeks, either with or without sh-Sestrin2. The effects of H₂S treatment on myocardial function, tissue structure, and myocardial cell apoptosis were assessed. Furthermore, the CCK-8 assay was used to detect the cell viability induced by TGF-β. Cellular oxidative stress levels were measured by the ELISA method. Western blotting was applied to determine the protein expression levels of Collagen I, Fibronectin, α-SMA, NLRP3, caspase-1, GSDMD-N, and Sestrin2.</div></div><div><h3>Results</h3><div>H₂S ameliorates HG-induced fibrosis, injury, pyroptosis, and inflammatory response of cardiac fibroblasts (CFs). H₂S inhibits Sestrin2 methylation and up-regulates its expression through DNMT3a. H₂S ameliorates HG-induced CFs pyroptosis and fibrosis through Sestrin2. Sestrin2 regulates HG-induced CFs pyroptosis and fibrosis through the TLR4/MyD88/NF-κB pathway. The myocardial tissue injury was improved after H₂S treatment, and the results of the H₂S treatment were reversed after knockdown of Sestrin2. In addition, TGF-β1 can induce an increase in the activity of cardiac fibroblasts and enhance cellular oxidative stress. Meanwhile, it significantly upregulates the expression of Collagen I, Fibronectin, α-SMA, as well as NLRP3, caspase-1, and GSDMD-N, and remarkably downregulates the expression of Sestrin2. However, H₂S intervention can reverse the aforementioned phenomena.</div></div><div><h3>Conclusion</h3><div>H₂S can suppress pyroptosis and ameliorate diabetic MF by inhibiting DNMT3a-mediated DNA methylation of Sestrin2 promoter through the TLR4/MyD88/NF-κB pathway.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"774 ","pages":"Article 110605"},"PeriodicalIF":3.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144991451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differential modulation of human lysozyme aggregation by sugar and derivatives: a biophysical insight","authors":"Murtaza Hussain,&nbsp;Md Nadir Hassan,&nbsp;Wajeeha Rao,&nbsp;Waseem Ahmad Siddiqui,&nbsp;Rizwan Hasan Khan","doi":"10.1016/j.abb.2025.110604","DOIUrl":"10.1016/j.abb.2025.110604","url":null,"abstract":"<div><div>Human Lysozyme, an essential enzyme within the innate immune system, is particularly vulnerable to glycation, resulting in structural modifications and aggregation. This study was conducted to examine the effects of Glucose, Fructose, Xylose, and Methylglyoxal on the glycation of human lysozyme and the subsequent aggregation that occurs. To evaluate conformational changes, CD spectroscopy was utilized, while glycation levels were quantified using AGE-specific fluorescence, NBT assay, and Levine methods. The evaluation of hydrophobicity changes was performed through ANS dye binding, and the propensity for aggregation was assessed using the ThT binding assay. Additionally, further characterization was conducted using SDS-PAGE, Transmission electron microscopy (TEM), and confocal microscopy. The results indicated that glycation with all tested sugars and derivative led to conformational changes in lysozyme, accompanied by increased hydrophobicity and an enhanced tendency for aggregation. Notably, methylglyoxal and xylose demonstrated a greater likelihood of forming advanced glycation end products. The aggregation of glycated lysozyme was corroborated through SDS-PAGE, TEM, and confocal microscopy analyses. Furthermore, it was observed that glycation adversely affected the lytic activity of lysozyme. These findings underscore the negative impact of glycation on the structure, function, and aggregation of lysozyme. A comprehensive understanding of the mechanisms driving glycation-induced aggregation may facilitate the advancement of therapeutic strategies aimed at addressing diseases associated with lysozyme dysfunction and glycation.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"773 ","pages":"Article 110604"},"PeriodicalIF":3.0,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144932545","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MALAT1 elevates the secretion of Th2 cytokines via miR-422a/NUP155 axis in allergic rhinitis mice","authors":"Xu Zhang ,&nbsp;Rui Yang ,&nbsp;Daoming Bai,&nbsp;Mengyuan Liu,&nbsp;Xinyu Huang,&nbsp;Wei Wan,&nbsp;Chunping Yang","doi":"10.1016/j.abb.2025.110603","DOIUrl":"10.1016/j.abb.2025.110603","url":null,"abstract":"<div><div>MALAT1 is one of the most well-studied lncRNAs in various diseases. This work attempted to investigate whether long non-coding RNA MALAT1 participate in the development of allergic rhinitis (AR). In this work, nasal mucosal tissues were obtained from AR patients. The mouse AR model was established by sensitization and challenge with ovalbumin. MALAT1, GATA3 and NUP155 were up-regulated, miR-422a was down-regulated in AR patients and mice. The sneezing number, rubbing number and rhinorrhea were increased in AR mice as compared with normal mice. The levels of IL-4, IL-5, IL-9 and IL-13 were elevated in nasal lavage fluid of AR mice. MALAT1 deficiency repressed the secretion of Th2 cytokines in ILC2 cells, which was abrogated by NUP155 overexpression. NUP155 knockdown reversed the promotion of MALAT1 overexpression on the secretion of Th2 cytokines. Moreover, MALAT1 elevated NUP155 expression by sponging miR-422a. <em>In vivo</em>, MALAT1 silencing reduced the sneezing number, rubbing number and rhinorrhea, ameliorated damage of nasal mucosal tissues in AR mice. Similarly, NUP155 knockdown also significantly alleviated AR clinical symptoms, improved nasal mucosal pathology, and suppressed the secretion of Th2 cytokines <em>in vivo</em>. In conclusion, this work demonstrated that MALAT1 elevated the secretion of Th2 cytokines in ILC2 cells by regulating miR-422a/NUP155 axis, which contributed to AR progression. Thus, MALAT1 may be a potential target for AR treatment.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"773 ","pages":"Article 110603"},"PeriodicalIF":3.0,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144922279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}