BMB Reports最新文献_第2页

Neutrophils in MASLD and MASH. MASLD和MASH中的中性粒细胞。

IF 2.9 3区生物学

BMB Reports Pub Date : 2025-03-01

Sanjeeb Shrestha, Jae-Han Jeon, Chang-Won Hong

{"title":"Neutrophils in MASLD and MASH.","authors":"Sanjeeb Shrestha, Jae-Han Jeon, Chang-Won Hong","doi":"","DOIUrl":"","url":null,"abstract":"Metabolic Dysfunction Associated Steatotic Liver Disease (MASLD) and its progressive form, Metabolic Dysfunction Associated Steatohepatitis (MASH), represent significant health concerns associated with the metabolic syndrome. These conditions are characterized by excessive hepatic fat accumulation, inflammation, and potential progression to cirrhosis and hepatocellular carcinoma. Neutrophils are innate immune cells that play a pivotal role in the development of MASLD and MASH. They can infiltrate the hepatic microenvironment in response to inflammatory cytokines and damage associated molecular patterns (DAMPs) derived from the liver and exacerbate tissue damage by releasing of reactive oxygen species (ROS), cytokines, and neutrophil extracellular traps (NETs). Moreover, neutrophils can disrupt the metabolism of hepatocytes through key factors such as neutrophil elastase (NE) and human neutrophil peptides-1 (HNP-1), leading to inflammation and fibrosis, while myeloperoxidase (MPO) and lipocalin (LCN2) are involved in inflammatory and fibrotic processes. In contrast, neutrophils contribute to liver protection and repair through mechanisms involving microRNA-223 and matrix metalloproteinase 9 (MMP9). This dual role of neutrophils highlights their significance in the pathogenesis of MASLD and MASH. This review summarizes current understanding from recent studies on the involvement of neutrophils in MASLD and MASH. Understanding complex roles of neutrophils within the liver's unique microenvironment offers insights into novel therapeutic strategies, emphasizing the need for further research to explore neutrophil-targeted interventions for managing MASLD and MASH. [BMB Reports 2025; 58(3): 116-123].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"116-123"},"PeriodicalIF":2.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11955729/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142930678","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Monocyte activation test (MAT) as an ethical alternative to animal testing.

IF 2.9 3区生物学

BMB Reports Pub Date : 2025-03-01

Yeram Jeon, Soyoung Jeon, Ji-Youn Lim, Hyungjung Koh, Chan Woong Choi, Su Kyoung Seong, Boksik Cha, Wantae Kim

引用次数: 0

GPR40-full agonist AM1638 alleviates palmitate-induced oxidative damage in H9c2 cells via an AMPK-dependent pathway. GPR40-full激动剂AM1638通过ampk依赖性途径减轻棕榈酸诱导的H9c2细胞氧化损伤。

IF 2.9 3区生物学

BMB Reports Pub Date : 2025-03-01

SukHwan Yun, Joo Won Kim, Min Jeong Park, Eyun Song, Soo Yeon Jang, Ahreum Jang, Kyung Mook Choi, Sei Hyun Baik, Hwan-Jin Hwang, Hye Jin Yoo

{"title":"GPR40-full agonist AM1638 alleviates palmitate-induced oxidative damage in H9c2 cells via an AMPK-dependent pathway.","authors":"SukHwan Yun, Joo Won Kim, Min Jeong Park, Eyun Song, Soo Yeon Jang, Ahreum Jang, Kyung Mook Choi, Sei Hyun Baik, Hwan-Jin Hwang, Hye Jin Yoo","doi":"","DOIUrl":"","url":null,"abstract":"G protein-coupled receptor 40 (GPR40) is gaining recognition as a potential therapeutic target for several metabolic disturbances, such as hyperglycemia and excessive inflammation. GPR40 is expressed in various tissues, including the heart; however, its specific roles in cardiomyocytes remain unknown. The objective of the present study was to investigate whether treatment with AM1638, a GPR40-full agonist, reduces palmitate-mediated cell damage in H9c2 rat cardiomyocytes. AM1638 treatment increased the phosphorylation of adenosine monophosphate-activated protein kinase (AMPK) and expression levels of the antioxidant molecules heme oxygenase-1 (HO-1) and nicotinamide adenine dinucleotide phosphate: quinone oxidoreductase-1 (NQO1). Palmitate-mediated superoxide production and levels of 4-hydroxynonenal, a biomarker of oxidative stress, decreased after treatment with AM1638. Notably, palmitate-mediated disruption of mitochondrial membrane potential, lower levels of mitochondrial complex protein, and failure of adenosine triphosphate production were all recovered by treatment with AM1638. Moreover, AM1638 blocked palmitate-mediated caspase-3 cleavage and nuclear fragmentation, thereby improving cell viability. However, these AM1638-mediated beneficial effects were abrogated by treatment with Compound C, an AMPK inhibitor. These results demonstrate that AM1638, a GPR40-full agonist, ameliorates palmitate-mediated oxidative stress in H9c2 cells in an AMPK-dependent manner. [BMB Reports 2025; 58(3): 133-139].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"133-139"},"PeriodicalIF":2.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11955733/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142930676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

JMJD4 promotes tumor progression via inhibition of the PDCD5-TP53 pathway. JMJD4 通过抑制 PDCD5-TP53 通路促进肿瘤进展。

IF 2.9 3区生物学

BMB Reports Pub Date : 2025-02-01

Hyunsik Kim, Subhin Jang, Soo Yeon Lee, Jae-Hwan Kwon, Seunghee Byun, Jung-Yoon Yoo, Sungryul Yu, Soo-Yeon Park, Ho-Geun Yoon

{"title":"JMJD4 promotes tumor progression via inhibition of the PDCD5-TP53 pathway.","authors":"Hyunsik Kim, Subhin Jang, Soo Yeon Lee, Jae-Hwan Kwon, Seunghee Byun, Jung-Yoon Yoo, Sungryul Yu, Soo-Yeon Park, Ho-Geun Yoon","doi":"","DOIUrl":"","url":null,"abstract":"Programmed cell death 5 (PDCD5) regulates cell death and suppresses tumor progression. Since the stability and nuclear translocation of PDCD5 are regulated by TP53-dependent cell death stimuli, knowledge of the regulatory mechanism of PDCD5 function is required to better understand the TP53-signaling pathway. We identified Jumonji domain-containing protein 4 (JMJD4) to be a PDCD5-interacting protein using liquid chromatography- mass spectrometry (LC-MS). Interestingly, JMJD4 upregulates cell proliferation and chemo-resistance under genotoxic stress conditions by colony-formation assay and decreases TP53-related apoptotic genes (BAX, PUMA) by suppressing protein levels of PDCD5. Additionally, using the Cancer Genome Atlas and the Gene Expression Omnibus database to confirm the clinical correlation between JMJD4 and cancer patients, we verified that JMJD4 is associated with a poor prognosis in colon cancer and lung cancer patients. Therefore, this study demonstrates that JMJD4 directly interacts with PDCD5, regulates cancer cell death negatively, and could be a potential therapeutic target for cancer development. [BMB Reports 2025; 58(2): 64-69].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"64-69"},"PeriodicalIF":2.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11875742/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142680670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Development of a prime editor with improved editing efficiency in Arabidopsis. 提高拟南芥编辑效率的主编辑器的研制。

IF 2.9 3区生物学

BMB Reports Pub Date : 2025-02-01

Yeong Yeop Jeong, Cheljong Hong, Jun Hee Han, Sangsu Bae, Pil Joon Seo

引用次数: 0

Plant-derived extracellular vesicles as nanocarriers for combination therapy enhancing paclitaxel-based regimens in breast cancer.

IF 2.9 3区生物学

BMB Reports Pub Date : 2025-02-01

Youngcheon Song, Hyunseok Kong, Soohwan Oh, Sang Bum Kim

{"title":"Plant-derived extracellular vesicles as nanocarriers for combination therapy enhancing paclitaxel-based regimens in breast cancer.","authors":"Youngcheon Song, Hyunseok Kong, Soohwan Oh, Sang Bum Kim","doi":"","DOIUrl":"","url":null,"abstract":"Breast cancer remains a leading cause of morbidity and mortality worldwide. Triple-negative breast cancer (TNBC) presents unique challenges owing to its aggressiveness and limited treatment options. Paclitaxel-based chemotherapy is widely used in breast cancer treatment. However, its efficacy is often limited by toxicity, multidrug resistance, and lack of targeted delivery. In response to these challenges, recent studies have focused on the use of extracellular vesicles (EVs), particularly plant-derived EVs, as innovative drug delivery systems capable of enhancing therapeutic outcomes and reducing adverse effects. Plant-derived EVs offer significant advantages owing to their biocompatibility, low immunogenicity, and scalability. They provide a natural platform for delivering chemotherapeutics such as paclitaxel and doxorubicin directly to tumor cells. This review explores the therapeutic potential of plant-derived EVs in breast cancer treatment, focusing on TNBC by examining their ability to improve drug stability, bioavailability, and selective targeting of cancer cells. Key studies on EVs derived from plants such as grapefruit, ginger, and tea leaves have demonstrated their capacity to deliver chemotherapeutic agents effectively while mitigating common side effects associated with conventional delivery methods. Although the use of plantderived EVs is still in early stages of research, findings suggest that that these nanocarriers can serve as transformative tools in oncology, providing a versatile and efficient platform for precise cancer treatment. This review highlights current landscape of research on plant-derived EVs, their application in breast cancer therapy, and future directions required to translate these findings into clinical practice. [BMB Reports 2025; 58(2): 53-63].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"53-63"},"PeriodicalIF":2.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11875746/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143466800","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Establishment and characterization of endometrial organoids from different placental types. 不同胎盘类型子宫内膜类器官的建立与表征。

IF 2.9 3区生物学

BMB Reports Pub Date : 2025-02-01

Dong-Hyeok Kwon, Byeonghwi Lim, Sung-Yeon Lee, Sung-Ho Won, Goo Jang

{"title":"Establishment and characterization of endometrial organoids from different placental types.","authors":"Dong-Hyeok Kwon, Byeonghwi Lim, Sung-Yeon Lee, Sung-Ho Won, Goo Jang","doi":"","DOIUrl":"","url":null,"abstract":"Understanding molecular characteristics and metabolic processes of the mammalian endometrium is crucial for advancing biological research, particularly in veterinary obstetrics and pathology. This study established and analyzed organoids from endometrial epithelial stem cells of five mammals with different placental types: cows (cotyledonary), dogs and cats (zonary), pigs (diffuse), and rats (discoid). Organoids from these five species were maintained for over 13 passages, frozen, and thawed. Pathological analysis confirmed that they retained characteristics of their original tissues. Furthermore, integrative transcriptome analysis of organoids and tissues from the five species highlighted key pathways such as PI3K-Akt signaling and extracellular matrix-receptor interaction known to be crucial in cancer research. Although genes associated with vascular smooth muscle contraction were downregulated, these organoids exhibited significant activities of genes involved in hormone metabolism. In conclusion, our study achieved stable establishment of endometrial organoids from five mammals with different placental types, offering foundational data for organoid research. In the future, these organoids are suitable models for investigating uterine physiology and diseases and for developing potential therapies. [BMB Reports 2025; 58(2): 95-103].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"95-103"},"PeriodicalIF":2.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11875743/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142833799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Wnt5a exacerbates pathological bone features and trabecular bone loss in curdlan-injected SKG mice via osteoclast activation. Wnt5a通过破骨细胞激活，在注射胶原蛋白的SKG小鼠中加剧病理性骨特征和小梁骨丢失。

IF 2.9 3区生物学

BMB Reports Pub Date : 2025-02-01

Min Whangbo, Eunae Ko, Dongju Kim, Chanhyeok Jeon, Hye-Ryeong Jo, Seung Hoon Lee, Jeehee Youn, Sungsin Jo, Tae-Hwan Kim

{"title":"Wnt5a exacerbates pathological bone features and trabecular bone loss in curdlan-injected SKG mice via osteoclast activation.","authors":"Min Whangbo, Eunae Ko, Dongju Kim, Chanhyeok Jeon, Hye-Ryeong Jo, Seung Hoon Lee, Jeehee Youn, Sungsin Jo, Tae-Hwan Kim","doi":"","DOIUrl":"","url":null,"abstract":"Many studies on osteoblasts have suggested that Wnt5a plays a crucial role in excessive osteoblast activity, which is responsible for ectopic new bone formation, but research on osteoclasts in ankylosing spondylitis (AS) remains relatively limited. This study aimed to explore whether Wnt5a influences osteoclastmediated bone resorption in curdlan-injected SKG mice, a model that mimics AS. Compared to the Vehicle group, the Wnt5a treatment group exhibited statistically higher clinical arthritis scores and increased hindpaw thickness values. Micro- computed tomography (microCT) analysis of hindpaws revealed a significant increase in inflamed and ectopic bone density in the Wnt5a-treated group compared to the Vehicle group. Histological examination also showed pronounced inflammation and structural bone damage in the bone marrow of ankles in the Wnt5a-treated group. Intriguingly, microCT analysis of the femur revealed that trabecular bone loss was markedly observed in the Wnt5a-treated group. Both the number of TRAP-positive osteoclasts and their activity were statistically greater in the Wnt5a-treated group compared to the Vehicle group. Serum markers of bone resorption, but not bone formation, were also significantly elevated in the Wnt5a-treated group. Notably, promotion of osteoclast differentiation by Wnt5a was inhibited following treatment with anti-Wnt5a. These findings suggest that targeting Wnt5a could be a promising strategy for mitigating pathological bone features in AS by modulating osteoclast activity. [BMB Reports 2025; 58(2): 75-81].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"75-81"},"PeriodicalIF":2.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11875747/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142833883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Erratum to: Differential roles of N- and C-terminal LIR motifs in the catalytic activity and membrane targeting of RavZ and ATG4B proteins. 勘误：N端和C端LIR基团在RavZ和ATG4B蛋白的催化活性和膜靶向中的不同作用

IF 2.9 3区生物学

BMB Reports Pub Date : 2025-02-01

Sang-Won Park, Ju-Hui Park, Haneul Choi, Pureum Jeon, Seung-Hwan Lee, Won-Dong Shin, Hun-Joo Kim, Jin-A Lee, Deok-Jin Jang

{"title":"Erratum to: Differential roles of N- and C-terminal LIR motifs in the catalytic activity and membrane targeting of RavZ and ATG4B proteins.","authors":"Sang-Won Park, Ju-Hui Park, Haneul Choi, Pureum Jeon, Seung-Hwan Lee, Won-Dong Shin, Hun-Joo Kim, Jin-A Lee, Deok-Jin Jang","doi":"","DOIUrl":"","url":null,"abstract":"[Erratum to: BMB Reports 2024; 57(11): 497-502, PMID: 39384175, PMCID: PMC11608851] The BMB Reports would like to issue a correction to an article published in BMB Rep. 57(11): 497-502, titled \"Differential roles of N- and C-terminal LIR motifs in the catalytic activity and membrane targeting of RavZ and ATG4B proteins\". The original acknowledgment contained incorrect grant information. This has now been corrected at the authors' request as follows: The work was supported by the Science Research Center Program of the National Research Foundation NRF (2020R1A5A1019023); Neurological Disorder Research Program of the NRF (2020M3E5D9079911); Basic research program of the NRF (2023R1A2C2007082) to JAL. D.-J.J. was supported by the Basic Research Program of NRF (2022R1F1A1066552), and the NRF grant funded by the Korea government (MSIT) (RS-2023-00218515). Specifically, the grant number has been updated from [2023R1A2C2008092] to [2023R1A2C2007082]. The authors apologize for any inconvenience or confusion this error may have caused. The ACKNOWLEDGEMENTS section in the original PDF version has been updated accordingly.","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":"58 2","pages":"104"},"PeriodicalIF":2.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11875745/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143482142","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

PGC1α is a key regulator of erastin-induced mitochondrial dysfunction during ferroptotic cell death. PGC1α是内皮素诱导的铁细胞死亡过程中线粒体功能障碍的关键调节因子。

IF 2.9 3区生物学

BMB Reports Pub Date : 2025-02-01

Byeong Geun Seok, Eunhee Park, Young-Jun Park, Hyuk Nam Kwon, Su Wol Chung

{"title":"PGC1α is a key regulator of erastin-induced mitochondrial dysfunction during ferroptotic cell death.","authors":"Byeong Geun Seok, Eunhee Park, Young-Jun Park, Hyuk Nam Kwon, Su Wol Chung","doi":"","DOIUrl":"","url":null,"abstract":"A type of programmed cell death called ferroptosis is defined by increased iron-dependent lipid peroxidation. Mitochondria play a central role in iron metabolism. Mitochondrial defects include decreased cristae density, membrane rupture, and decreased mitochondrial membrane density, which occur as a result of ferroptosis. One of the important regulator of mitochondrial biogenesis is PGC1α. While recent studies have begun to explore the association between PGC1α and ferroptosis, the specific role of PGC1α in erastin-induced mitochondrial dysfunction during ferroptotic cell death has not been fully elucidated. In this study, we demonstrate for the first time that PGC1α is a key regulator of erastin-induced mitochondrial-dependent lipid peroxidation and dysfunction during ferroptosis in HT1080 fibrosarcoma cells. In this study, we examined PGC1α function in ferroptosis. Erastin, an inducer of ferroptosis, boosted the expression of PGC1α. Moreover, PGC1α down-regulation reduced erastin-induced ferroptosis. The most important biochemical feature of ferroptosis is the increase in iron ion (Fe2＋)-dependent lipid peroxide (LOOH) concentration. Mitochondrial-dependent lipid peroxidation was abolished by PGC1α downregulation. In addition, PGC1α was induced during mitochondrial dysfunction in erastin-induced ferroptosis. Mitochondrial membrane potential loss and mitochondrial ROS production associated with erastin-induced mitochondrial dysfunction were blocked by PGC1α inhibition. In addition, erastin-induced lipid peroxidation in HT1080 fibrosarcoma cells was regulated by PGC1α inhibitor. This phenomenon was also consistent in HT1080 cells transfected with PGC1α shRNA. Taken together, these results suggest that PGC1α is a key factor in erastin-induced mitochondrial-dependent lipid peroxidation and dysfunction during ferroptosis cell death. [BMB Reports 2025; 58(2): 89-92].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"89-94"},"PeriodicalIF":2.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11875744/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142833826","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0