Biochemistry and Cell Biology最新文献_第10页

A reliable Western blot workflow with improved dynamic range for the detection of myelin proteins in murine brain. 一种可靠的western blot工作流程，具有改进的动态范围，用于检测小鼠大脑中的髓磷脂蛋白。

IF 2.1 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2025-0093

Victor P Liu, Shaheer Lakhani, Kendra L Furber

{"title":"A reliable Western blot workflow with improved dynamic range for the detection of myelin proteins in murine brain.","authors":"Victor P Liu, Shaheer Lakhani, Kendra L Furber","doi":"10.1139/bcb-2025-0093","DOIUrl":"10.1139/bcb-2025-0093","url":null,"abstract":"Myelin is a highly structured multilamellar sheath produced by oligodendrocytes, which insulates neuronal axons to facilitate neurotransmission. Maturation of oligodendrocytes in cortical regions of the developing murine brain occurs postnatally and corresponds to the marked upregulation of myelin-specific genes. Western blotting is a conventional technique used to study protein expression but historically has only been considered semiquantitative. This study aims to optimize a Western blot workflow for the quantification of myelin proteins in murine brain, including the examination of the following parameters: sample preparation, electrophoretic transfer conditions, detection parameters, data normalization, and linear dynamic range. As a proof of principle, the optimized protocol was employed to characterize both the absolute and relative expression of myelin oligodendrocyte glycoprotein (MOG) throughout neurodevelopment. A dynamic loading paradigm, which varied total protein load across different age groups to ensure antigen detection remained in the linear dynamic range of the assay, showed a greater relative increase in expression when compared to standard loading paradigm. This approach resulted in comparable MOG expression profiles from both absolute and relative quantification. The optimized Western blot workflow will facilitate protein quantification and will improve data reproducibility when investigating the molecular mechanisms of myelination in development, aging, and disease.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-13"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144289382","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}

引用次数: 0

Subacute exposure to aluminium chloride induces cytotoxicity and oxidative stress in rat erythrocytes: a dose-dependent study. 亚急性暴露于氯化铝诱导大鼠红细胞细胞毒性和氧化应激：剂量依赖性研究。

IF 2.1 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2024-0236

Farha Shahabuddin, Samina Naseem, Farah Khan

{"title":"Subacute exposure to aluminium chloride induces cytotoxicity and oxidative stress in rat erythrocytes: a dose-dependent study.","authors":"Farha Shahabuddin, Samina Naseem, Farah Khan","doi":"10.1139/bcb-2024-0236","DOIUrl":"10.1139/bcb-2024-0236","url":null,"abstract":"Aluminium (Al) toxicity has attracted considerable interest due to its bioavailability, environmental persistence, and adverse health effects. The present study investigates the effect of Al on rat erythrocytes under in vivo conditions. Rats were administered 0 (control), 25 (Al 1), 35 (Al 2), 45 (Al 3), and 55 (Al 4) mg/kg b.wt. of AlCl3 orally for 30 days. Hemolysates were prepared from different experimental groups and assayed for various biochemical parameters. AlCl3 administration significantly increased protein oxidation and lipid peroxidation, while decreasing total sulfhydryl and glutathione levels in rat erythrocytes. Methemoglobin level was increased and methemoglobin reductase activity was decreased upon AlCl3 treatment. Prolonged AlCl3 exposure inhibited the activities of antioxidant enzymes, and lowered the cells' antioxidant power. It also caused an increase in H2O2 and NO levels showing generation of oxidative and nitrosative stress. AlCl3 intoxication adversely affected the membrane-bound and metabolic enzyme activities. Alterations in all the biochemical parameters were found in an AlCl3 dose-dependent manner. Scanning electron microscopy showed gross morphological changes in erythrocytes from discocytes to acanthocytes and echinocytes, further supporting the damaging effect of aluminium. The aluminium-induced oxidative stress seems to be the key mechanism of damage to the cellular components that could lead to red cell senescence.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-14"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144186429","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}

引用次数: 0

Quercetin alleviates the progression of chronic rhinosinusitis by affecting nasal mucosal epithelial remodeling, inflammation, and Treg/Th17 imbalance. 槲皮素通过影响鼻黏膜上皮重塑、炎症和Treg/Th17失衡来缓解慢性鼻窦炎的进展。

IF 2.1 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2025-0049

Xiaopeng Qu, Pengyu Tao, Jiajia Dong, Lingzhao Meng

{"title":"Quercetin alleviates the progression of chronic rhinosinusitis by affecting nasal mucosal epithelial remodeling, inflammation, and Treg/Th17 imbalance.","authors":"Xiaopeng Qu, Pengyu Tao, Jiajia Dong, Lingzhao Meng","doi":"10.1139/bcb-2025-0049","DOIUrl":"10.1139/bcb-2025-0049","url":null,"abstract":"Nasal mucosal epithelial tissue remodeling and persist inflammation are related to the development of chronic rhinosinusitis (CRS). Quercetin possesses multiple biological properties in several inflammatory diseases. However, its roles in CRS remain unclear. In this study, Serumstaphylococcus aureus enterotoxin B (SEB) increased inflammatory response in human nasal epithelial cells (hNECs), which was reversed by quercetin. Moreover, quercetin inhibited SEB-evoked epithelial-mesenchymal transition (EMT) in hNECs by increasing EMT marker E-cadherin and decreasing N-cadherin expression. Concomitantly, SEB-induced increases in transcripts and release of MMP-9 were reduced by quercetin. Mechanistically, quercetin inhibited SEB-induced activation of the TLR2-NF-kB axis in hNECs. Moreover, restoring TLR2 signaling reversed quercetin-mediated inhibition of SEB-induced inflammation, EMT and MMP-9 expression. In vivo, quercetin attenuated histopathological changes of nasal mucosal tissues in Staphylococcus aureus-constructed CRS mice. Concomitantly, quercetin alleviated inflammatory response and nasal mucosal remodeling by suppressing EMT and MMP-9 levels. Additionally, quercetin ameliorated imbalance of Treg/Th17 proportions. Notably, quercetin suppressed activation of the TLR2-NF-kB axis, while restoring this signaling reversed quercetin-mediated protection against CRS. Thus, quercetin may attenuate pathological progression of CRS by inhibiting nasal mucosal tissue remodeling, inflammation and Treg/Th17 imbalance, which may be associated with inhibition of TLR2-NF-kB axis, supporting a promising therapeutic agent for CRS.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-11"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144551836","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}

引用次数: 0

Omega-3 polyunsaturated fatty acids modify glucose metabolism in THP-1 monocytes. Omega-3多不饱和脂肪酸改变THP-1单核细胞的葡萄糖代谢。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2024-0202

Michael J Byun, Roni Armon, Tamiris F G Souza, Hope D Anderson, Ayesha Saleem, Samantha D Pauls

{"title":"Omega-3 polyunsaturated fatty acids modify glucose metabolism in THP-1 monocytes.","authors":"Michael J Byun, Roni Armon, Tamiris F G Souza, Hope D Anderson, Ayesha Saleem, Samantha D Pauls","doi":"10.1139/bcb-2024-0202","DOIUrl":"10.1139/bcb-2024-0202","url":null,"abstract":"Chronic inflammation is a driving factor in diseases like obesity and type 2 diabetes. Enhanced cellular glucose metabolism may contribute to heightened immune activation. A human supplementation trial showed that the n-3 PUFA α-linolenic acid (ALA) reduced oxidative phosphorylation in monocytes. Our objective here is to assess the direct effects of ALA and docosahexaenoic acid (DHA) on glucose metabolism in a cell culture model and to explore possible molecular mechanisms. THP-1 monocytes were treated with 10-40 µmol/L of ALA or DHA and compared with vehicle and oleic acid controls. The Seahorse XFe24 and Oroboros O2k Oxygraph systems were used to approximate catabolic rates in the presence of glucose. Both ALA and DHA reduced oxidative phosphorylation. We identified pyruvate dehydrogenase kinase 4 (PDK4) as a possible mechanistic candidate explaining the effect of DHA. Additionally, both n-3 PUFAs reduced lipopolysaccharides-induced IL-1β production, while only DHA increased reactive oxygen species to a small but significant extent. Our data suggest that ALA and DHA trigger a re-wiring of bioenergetic pathways in monocytes, possibly via the upregulation of PDK4. Given the close relationship between cell metabolism and immune cell activation, this may represent a novel mechanism by which n-3 fatty acids modulate immune function and inflammation.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-10"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143121857","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}

引用次数: 0

CD38 deficiency prevents diabetic nephropathy by inhibiting lipid accumulation and oxidative stress through activation of the SIRT3 pathway. CD38 缺乏症可通过激活 SIRT3 途径抑制脂质积累和氧化应激，从而预防糖尿病肾病。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 Epub Date: 2024-08-08 DOI: 10.1139/bcb-2024-0058

Ling-Fang Wang, Qian Li, Jia Le Zhao, Ke Wen, Ya-Ting Zhang, Qi-Hang Zhao, Qi Ding, Jia-Hui Li, Xiao-Hui Guan, Yun-Fei Xiao, Ke-Yu Deng, Hong-Bo Xin

{"title":"CD38 deficiency prevents diabetic nephropathy by inhibiting lipid accumulation and oxidative stress through activation of the SIRT3 pathway.","authors":"Ling-Fang Wang, Qian Li, Jia Le Zhao, Ke Wen, Ya-Ting Zhang, Qi-Hang Zhao, Qi Ding, Jia-Hui Li, Xiao-Hui Guan, Yun-Fei Xiao, Ke-Yu Deng, Hong-Bo Xin","doi":"10.1139/bcb-2024-0058","DOIUrl":"10.1139/bcb-2024-0058","url":null,"abstract":"Diabetic nephropathy (DN) is one of the most common complications of diabetes. Our previous study showed that CD38 knockout (CD38KO) mice had protective effects on many diseases. However, the roles and mechanisms of CD38 in DN remain unknown. Here, DN mice were generated by high-fat diet (HFD) feeding plus streptozotocin (STZ) injection in male CD38KO and CD38flox mice. Mesangial cells (SV40 MES 13 cells) were used to mimic the injury of DN with palPagination Donemitic acid (PA) treatment in vitro. Our results showed that CD38 expression was significantly increased in kidney of diabetic CD38flox mice and SV40 MES 13 cells treated with PA. CD38KO mice were significantly resistant to diabetes-induced renal injury. Moreover, CD38 deficiency markedly decreased HFD/STZ-induced lipid accumulation, fibrosis, and oxidative stress in kidney tissue. In contrast, overexpression of CD38 aggravated PA-induced lipid accumulation and oxidative stress. CD38 deficiency increased expression of SIRT3, while overexpression of CD38 decreased its expression. More importantly, 3-TYP, an inhibitor of SIRT3, significantly enhanced PA-induced lipid accumulation and oxidative stress in CD38 overexpressing cell lines. In conclusion, our results demonstrated that CD38 deficiency prevented DN by inhibiting lipid accumulation and oxidative stress through activation of the SIRT3 pathway.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-12"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141905787","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}

引用次数: 0

Retraction: Long noncoding RNA HIF1A-AS2 facilitates cell survival and migration by sponging miR-33b-5p to modulate SIRT6 expression in osteosarcoma. 缩稿：长链非编码RNA HIF1A-AS2通过海绵miR-33b-5p调节SIRT6在骨肉瘤中的表达，促进细胞存活和迁移。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2025-0019

引用次数: 0

WDR4 promotes colorectal cancer progression by activating the GSK3β/β-catenin pathway. WDR4通过激活GSK3β/β-catenin通路促进结直肠癌的进展。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2024-0168

Hongyu Wang, Liyang Liang, Yanfei Wang, Xuan Zhong, Chao Zhang, Zhipeng Liu, Jinzhong Liu, Wanning Hu

{"title":"WDR4 promotes colorectal cancer progression by activating the GSK3β/β-catenin pathway.","authors":"Hongyu Wang, Liyang Liang, Yanfei Wang, Xuan Zhong, Chao Zhang, Zhipeng Liu, Jinzhong Liu, Wanning Hu","doi":"10.1139/bcb-2024-0168","DOIUrl":"10.1139/bcb-2024-0168","url":null,"abstract":"WD repeat domain 4 (WDR4) has been reported to promote tumor metastasis in various cancers. However, its precise function in colorectal cancer (CRC) has not been reported yet. Herein, the expression pattern of WDR4 in CRC was determined by analyzing Gene Expression Omnibus datasets (GSE110225, GSE127069, GSE156355, and GSE184093) and GEPIA online dataset. In vitro and in vivo experiments, including CCK-8, colony formation, flow cytometry, wound healing, transwell assays, and xenograft mouse models, were used to investigate the role of WDR4 in CRC. Firstly, data from Kaplan-Meier database showed that high expression of WDR4 was associated with the poor prognosis of CRC patients. Then, upregulation of WDR4 was confirmed in clinical CRC tissues. In vitro functional experiments suggested that overexpression of WDR4 promoted cell proliferation, migration, and invasion, while knockdown of WDR4 has the opposite effects. Also, the oncogenic role of WDR4 was also verified in in vivo experiments. CO-IP-LC/MS analysis uncovered that glycogen synthase kinase 3β (GSK3β) is the central protein that binds to WDR4. Mechanistically, WDR4 activated the β-catenin pathway by promoting GSK3β phosphorylation. This study demonstrates that WDR4 promotes CRC progression through activating GSK3β/β-catenin pathway, indicating that WDR4 might be a potential therapeutic target for CRC treatment.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-12"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514501","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}

引用次数: 0

A role for NFIB in SOX2 downregulation and epigenome accessibility changes due to long-term estrogen treatment of breast cancer epithelial cells. NFIB在乳腺癌上皮细胞长期雌激素治疗导致的SOX2下调和表观基因组可及性改变中的作用

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2024-0287

Luis E Abatti, Zoe E Gillespie, Patricia Lado-Fernández, Manuel Collado, Jennifer A Mitchell

{"title":"A role for NFIB in SOX2 downregulation and epigenome accessibility changes due to long-term estrogen treatment of breast cancer epithelial cells.","authors":"Luis E Abatti, Zoe E Gillespie, Patricia Lado-Fernández, Manuel Collado, Jennifer A Mitchell","doi":"10.1139/bcb-2024-0287","DOIUrl":"10.1139/bcb-2024-0287","url":null,"abstract":"Estrogen (E2) regulates the differentiation and proliferation of mammary progenitor cells by modulating the transcription of multiple genes. One of the genes that is downregulated by E2 is SOX2, a transcription factor associated with stem and progenitor cells that is overexpressed during breast tumourigenesis. To elucidate the mechanisms underlying E2-mediated SOX2 repression, we investigated epigenome and transcriptome changes following short- and long-term E2 exposure in breast cancer cells. We found that short-term E2 exposure reduces chromatin accessibility at the downstream SOX2 SRR134 enhancer, decreasing SOX2 expression. In contrast, long-term E2 exposure completely represses SOX2 transcription while maintaining accessibility at the SRR124-134 enhancer cluster, keeping it poised for reactivation. This repression was accompanied by widespread epigenome and transcriptome changes associated with commitment towards a more differentiated and less invasive luminal phenotype. Finally, we identified a role for the transcription factor NFIB in this process, suggesting it collaborates with the estrogen receptor to mediate SOX2 repression and genome-wide epigenome accessibility changes.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-14"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514410","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}

引用次数: 0

Perturbation of calcium homeostasis invokes eryptosis-like cell death in enucleated bone marrow stem cells. 扰乱钙稳态会导致无核骨髓干细胞发生红细胞增多症样细胞死亡。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 Epub Date: 2024-11-18 DOI: 10.1139/bcb-2024-0106

Wei Yan, Ruolan Wu, Yingying Lee, Liqun Xu, Xiao Li, Junwei Li, Ronghao Deng, Xing Fan, Yilang Wu, Haibao Zhu, Aihua Mao, Jianxin Shen, Chi-Ju Wei

{"title":"Perturbation of calcium homeostasis invokes eryptosis-like cell death in enucleated bone marrow stem cells.","authors":"Wei Yan, Ruolan Wu, Yingying Lee, Liqun Xu, Xiao Li, Junwei Li, Ronghao Deng, Xing Fan, Yilang Wu, Haibao Zhu, Aihua Mao, Jianxin Shen, Chi-Ju Wei","doi":"10.1139/bcb-2024-0106","DOIUrl":"10.1139/bcb-2024-0106","url":null,"abstract":"Enucleated cells, also known as cytoplasts, are valuable tools with a wide range of applications. However, their potential for bio-engineering is greatly restricted by the short lifespan. We postulated that the enucleation process damages the integrity of the plasma membrane and thus activates a cell death program(s). The results showed that a tiny hole was generated transiently on the plasma membrane when the nucleus was spun off, while force-gated ion channels were activated in response to the pulling by the nucleus. Influx of extracellular calcium stimulated the opening of calcium channels and the release of calcium from endoplasmic reticulum and mitochondria. Long lasting calcium transient increased protein phosphorylation and activated caspase 9 and calpain proteinase activities. Subsequently, mitochondria membrane permeability and Reactive Oxygen Species (ROS) levels were significantly elevated, which eventually led to eryptosis-like cell death. When extracellular calcium was maintained at optimal concentration, the lifespan of enucleated cells was extended; however, huge amounts of vacuoles appeared in the cytoplasm, possibly derived from enlarged autophagosomes. Inhibition of vacuolation by inhibitors of autophagy or in co-culture with primary muscle cells did not rescue cells dying from the paraptosis-like pathway. These results offer valuable insights for further investigation into the intricate mechanisms underlying enucleated cell death.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-11"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142646832","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}

引用次数: 0

The role of NEDD4L in metabolic dysfunction-associated fatty liver disease (MAFLD) by regulating ferroptosis via deubiquitinating the TGF-β receptor TβRII. NEDD4L通过TGF-β受体TβRII去泛素化调控铁凋亡在代谢功能障碍相关脂肪肝（MAFLD）中的作用

IF 2.1 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2025-0175

Fang Li, Jiayi Yao, Jianhua Yao, Yusen Mou, Dan Li, Limin Wei

{"title":"The role of NEDD4L in metabolic dysfunction-associated fatty liver disease (MAFLD) by regulating ferroptosis via deubiquitinating the TGF-β receptor TβRII.","authors":"Fang Li, Jiayi Yao, Jianhua Yao, Yusen Mou, Dan Li, Limin Wei","doi":"10.1139/bcb-2025-0175","DOIUrl":"10.1139/bcb-2025-0175","url":null,"abstract":"We explored the mechanism of E3 ubiquitin ligase neural precursor cell expressed developmentally down regulated 4-like protein (NEDD4L) mediating ferroptosis sensitivity through the transforming growth factor-beta1 (TGF-β1) signaling to regulate high-fat and high-sugar diet (HFHS)-induced liver injury in HFHS feeding-induced metabolic dysfunction-associated fatty liver disease (MAFLD) mice. NEDD4L was poorly expressed in liver tissues of HFHS-induced MAFLD mice. NEDD4L overexpression ameliorated HFHS-induced liver injury in MAFLD mice. Mechanistically, NEDD4L overexpression repressed ferroptosis sensitivity in liver tissues and ameliorated HFHS-induced liver injury in MAFLD mice. NEDD4L hindered the TGF-β1 signaling by mediating TβRII ubiquitin degradation. Activation of the TGF-β1 signaling partially abrogated NEDD4L overexpression-ameliorated ferroptosis in liver tissues and HFHS-induced liver injury of MAFLD mice. NEDD4L might hinder the TGF-β1 signaling and inhibit ferroptosis sensitivity by mediating TβRII ubiquitin degradation, thereby improving HFHS-induced liver injury in MAFLD mice.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":"103 ","pages":"1-14"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145755147","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}

引用次数: 0