International Journal of Biochemistry & Cell Biology最新文献

{"title":"Retraction notice to \"HDAC3 increases HMGB3 expression to facilitate the immune escape of breast cancer cells via down-regulating microRNA-130a-3p\" [Int. J. Biochem. Cell Biol. 135 (2021) 105967]","authors":"Zonglin Chen, Lei Pei, Danhua Zhang, Feng Xu, Enxiang Zhou, Xianyu Chen","doi":"10.1016/j.biocel.2024.106620","DOIUrl":"10.1016/j.biocel.2024.106620","url":null,"abstract":"","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"174 ","pages":"Article 106620"},"PeriodicalIF":3.4,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1357272524001122/pdfft?md5=78c9be35d05c4919fca9a7dd72bce10b&pid=1-s2.0-S1357272524001122-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141635638","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}

{"title":"Corrigendum to “Feijoa sellowiana derived natural Flavone exerts anti-cancer action displaying HDAC inhibitory activities” [Int. J. Biochem. Cell Biol. 39(10) (2007) 1902–1914]","authors":"Paola Bontempo , Luigi Mita , Marco Miceli , Antonella Doto , Angela Nebbioso , Floriana De Bellis , Mariarosaria Conte , Annunziata Minichiello , Fabio Manzo , Vincenzo Carafa , Adriana Basile , Daniela Rigano , Sergio Sorbo , Rosa Castaldo Cobianchi , Ettore Mariano Schiavone , Felicetto Ferrara , Mariacarla De Simone , MariaTeresa Vietri , Michele Cioffi , Vincenzo Sica , Anna Maria Molinari","doi":"10.1016/j.biocel.2024.106619","DOIUrl":"10.1016/j.biocel.2024.106619","url":null,"abstract":"","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"173 ","pages":"Article 106619"},"PeriodicalIF":3.4,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1357272524001110/pdfft?md5=7ccea3ac3b5a96292aa50eb2dd94b0ed&pid=1-s2.0-S1357272524001110-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141629212","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}

{"title":"Parsing the effect of co-culture with brain organoids on Diffuse Intrinsic Pontine Glioma (DIPG) using quantitative proteomics","authors":"Victoria G. Prior ,&nbsp;Simon Maksour ,&nbsp;Sara Miellet ,&nbsp;Amy J. Hulme ,&nbsp;Yuyan Chen ,&nbsp;Mehdi Mirzaei ,&nbsp;Yunqi Wu ,&nbsp;Mirella Dottori ,&nbsp;Geraldine M. O'Neill","doi":"10.1016/j.biocel.2024.106617","DOIUrl":"10.1016/j.biocel.2024.106617","url":null,"abstract":"<div><p>Diffuse Intrinsic Pontine Gliomas (DIPGs) are deadly brain cancers in children for which there is no effective treatment. This can partly be attributed to preclinical models that lack essential elements of the <em>in vivo</em> tissue environment, resulting in treatments that appear promising preclinically, but fail to result in effective cures. Recently developed co-culture models combining stem cell-derived brain organoids with brain cancer cells provide tissue dimensionality and a human-relevant tissue-like microenvironment. As these models are technically challenging, we aimed to establish whether interaction with the organoid influences DIPG biology and thus warrants their use. To address this question DIPG24 cells were cultured with pluripotent stem cell-derived cortical organoids. We created “mosaic” co-cultures enriched for tumour cell-neuronal cell interactions versus “assembloid” co-cultures enriched for tumour cell-tumour cell interactions. Sequential window acquisition of all theoretical mass spectra (SWATH-MS) was used to analyse the proteomes of DIPG fractions isolated by flow-assisted cell sorting. Control proteomes from DIPG spheroids were compared with DIPG cells isolated from mosaic and assembloid co-cultures. This suggested changes in cell interaction with the external environment reflected by decreased gene ontology terms associated with adhesion and extracellular matrix, and increased DNA synthesis and replication, in DIPG24 cells under either co-culture condition. By contrast, the mosaic co-culture was associated with neuron-specific brahma-associated factor (nBAF) complex signalling, a process associated with neuronal maturation. We propose that co-culture with brain organoids is a valuable tool to parse the contribution of the brain microenvironment to DIPG tumour biology.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"174 ","pages":"Article 106617"},"PeriodicalIF":3.4,"publicationDate":"2024-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1357272524001092/pdfft?md5=3c07bccfc573a9ab546a6dca7bf47c5f&pid=1-s2.0-S1357272524001092-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141621672","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}

{"title":"A brief review on recent advances in diagnostic and therapeutic applications of extracellular vesicles in cardiovascular disease","authors":"Diptimayee Das ,&nbsp;Ganesan Jothimani ,&nbsp;Antara Banerjee ,&nbsp;Amit Dey ,&nbsp;Asim K. Duttaroy ,&nbsp;Surajit Pathak","doi":"10.1016/j.biocel.2024.106616","DOIUrl":"10.1016/j.biocel.2024.106616","url":null,"abstract":"<div><p>Extracellular vesicles (EVs) are important mediators of intercellular communication within the cardiovascular system, playing essential roles in physiological homeostasis and contributing to the pathogenesis of various cardiovascular diseases (CVDs). However, their potential as diagnostic biomarkers and therapeutic agents in rare cardiovascular diseases, such as valvular heart disease (VHD) and cardiomyopathies, remains largely unexplored. This review comprehensively emphasizes recent advancements in extracellular vesicle research, explicitly highlighting their growing significance in diagnosing and potentially treating rare cardiovascular diseases, with a particular focus on valvular heart disease and cardiomyopathies. We highlight the potential of extracellular vesicle-based liquid biopsies as non-invasive tools for early disease detection and risk stratification, showcasing specific extracellular vesicle-associated biomarkers (proteins, microRNAs, lipids) with diagnostic and prognostic value. Furthermore, we discussed the therapeutic promise of extracellular vesicles derived from various sources, including stem cells and engineered extracellular vesicles, for cardiac repair and regeneration through their ability to modulate inflammation, promote angiogenesis, and reduce fibrosis. By integrating the findings and addressing critical knowledge gaps, this review aims to stimulate further research and innovation in extracellular vesicle-based diagnostics and therapeutics of cardiovascular disease.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"173 ","pages":"Article 106616"},"PeriodicalIF":3.4,"publicationDate":"2024-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1357272524001080/pdfft?md5=a30a3edb669717444a98a452f4dc5edf&pid=1-s2.0-S1357272524001080-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141591861","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}

{"title":"Bisphenol A (BPA) and neurological disorders: An overview","authors":"Sung-Ae Hyun,&nbsp;Minhan Ka","doi":"10.1016/j.biocel.2024.106614","DOIUrl":"10.1016/j.biocel.2024.106614","url":null,"abstract":"<div><p>The human body is commonly exposed to bisphenol A (BPA), which is widely used in consumer and industrial products. BPA is an endocrine-disrupting chemical that has adverse effects on human health. In particular, many studies have shown that BPA can cause various neurological disorders by affecting brain development and neural function during prenatal, infancy, childhood, and adulthood exposure. In this review, we discussed the correlation between BPA and neurological disorders based on molecular cell biology, neurophysiology, and behavioral studies of the effects of BPA on brain development and function. Recent studies, both animal and epidemiological, strongly indicate that BPA significantly impacts brain development and function. It hinders neural processes, such as proliferation, migration, and differentiation during development, affecting synaptic formation and activity. As a result, BPA is implicated in neurodevelopmental and neuropsychiatric disorders like <strong>autism spectrum disorder (ASD), attention-deficit hyperactivity disorder (ADHD),</strong> and schizophrenia.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"173 ","pages":"Article 106614"},"PeriodicalIF":3.4,"publicationDate":"2024-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1357272524001067/pdfft?md5=f8e71ca7ddffd50edbf73f66073b48ca&pid=1-s2.0-S1357272524001067-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141472122","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}

{"title":"A CEBPB/miR-32–5p/GATA6 axis promotes vascular calcification in type 2 diabetes","authors":"Zhibo Zhao ,&nbsp;Anqi Li ,&nbsp;Rong Zeng,&nbsp;Zhaolin Zeng,&nbsp;Linling Ou,&nbsp;Jingsong Cao,&nbsp;Jianghua Liu","doi":"10.1016/j.biocel.2024.106613","DOIUrl":"10.1016/j.biocel.2024.106613","url":null,"abstract":"<div><p>Vascular calcification in diabetes patients is a major independent risk factor for developing diabetic cardiovascular complications. However, the mechanisms by which diabetes leads to vascular calcification are complex and not yet fully understood. Our previous study revealed that miR-32–5p is a potential new diagnostic marker for coronary artery calcification. In this study, we found that miR-32–5p levels were significantly greater in the plasma of type 2 diabetes patients with coronary artery calcification and were positively correlated with the coronary artery calcification score. In type 2 diabetic mice, miR-32–5p levels were also elevated in the aorta, and knockout of miR-32–5p inhibited the osteogenic differentiation of vascular smooth muscle cells in vivo. Furthermore, overexpression of miR-32–5p promoted vascular smooth muscle cell calcification, while antagonism of miR-32–5p inhibited vascular smooth muscle cell calcification under high-glucose conditions. GATA binding protein 6 (GATA6) was identified as the key target gene through which miR-32–5p promotes vascular smooth muscle cell calcification. Overexpression of GATA6 antagonized the effects of miR-32–5p on vascular calcification. Additionally, high glucose levels were shown to induce the upregulation of miR-32–5p by activating CCAAT/enhancer binding protein beta (CEBPB). These results suggest that miR-32–5p is an important procalcification factor in vascular calcification associated with type 2 diabetes and identify the CEBPB/miR-32–5p/GATA6 axis as a potential biomarker and therapeutic target for preventing and treating vascular calcification in type 2 diabetes.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"173 ","pages":"Article 106613"},"PeriodicalIF":3.4,"publicationDate":"2024-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141443616","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":"TRPM8 affects relative “cooling and heating” of subcellular organelles in microglia in a context-dependent manner","authors":"Deep Shikha ,&nbsp;Young-Tae Chang ,&nbsp;Chandan Goswami","doi":"10.1016/j.biocel.2024.106615","DOIUrl":"10.1016/j.biocel.2024.106615","url":null,"abstract":"<div><p>Thermoregulation and thermal homeostasis at the cellular and subcellular organelle level are poorly understood events. In this work, we used BV2, a microglial cell line, and a series of thermo-sensitive subcellular organelle-specific probes to analyze the relative changes in the spatio-temporal temperatures of different subcellular organelles, both qualitatively and quantitatively. These methodologies allowed us to understand the thermal relationship of different subcellular organelles also. We modulated BV2 cells by pharmacological application of activator or inhibitor of TRPM8 ion channel (a cold-sensitive ion channel) and/or by treating the cells with LPS, a molecule that induces pathogen-associated molecular patterns (PAMPs) signaling. We demonstrate that the temperatures of individual organelles remain variable within a physiological range, yet vary in different conditions. We also demonstrate that treating BV2 cells by TRPM8 modulators and/or LPS alters the organelle temperatures in a specific and context-dependent manner. We show that TRPM8 modulation and/or LPS can alter the relationship of mitochondrial membrane potential to mitochondrial temperature. Our work suggests that mitochondrial temperature positively influences ER temperature and negatively influences Golgi temperature. Golgi temperature positively influences membrane temperature. This understanding of thermal relationships may be crucial for dissecting cellular structures, function, and stress signaling and may be relevant for different diseases.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"173 ","pages":"Article 106615"},"PeriodicalIF":3.4,"publicationDate":"2024-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141441057","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":"WeiNaiAn capsule attenuates intestinal mucosal injury and regulates gut microbiome in indomethacin-induced rat","authors":"Yanqiu Zheng ,&nbsp;Jinbin Song ,&nbsp;Lili Huang ,&nbsp;Guirong Chen ,&nbsp;Na Ning ,&nbsp;Qiuling Huang ,&nbsp;Shanshan Liu ,&nbsp;Yanli Wu ,&nbsp;Qun Du ,&nbsp;Jiazhong Cai ,&nbsp;Yanwu Li","doi":"10.1016/j.biocel.2024.106609","DOIUrl":"10.1016/j.biocel.2024.106609","url":null,"abstract":"<div><p>Indomethacin, as a non-steroidal anti-inflammatory drugs, is widely used in the clinic. However, it can cause severe injury to the gastrointestinal tract and the incidence is increasing. It has become an essential clinical problem in preventing intestinal damage. Teprenone has been reported to have a significant positive effect on intestinal mucosal lesions, but long-term use of teprenone can elicit adverse reactions. WeiNaiAn capsule is a traditional Chinese medicine formulation used widely in the treatment of gastric and duodenal mucosal injury. However, how WeiNaiAn protects against intestinal mucosal injury and its mechanism of action are not known. In this study, WeiNaiAn capsule or Teprenone treatment improved the intestinal mucosal pathological score and antioxidant level in indomethacin-induced rats. 16 S rRNA sequence data showed WeiNaiAn capsule reverted the structure community and replenished the beneficial bacteria. Furthermore, fingerprint analysis revealed multiple components of WeiNaiAn capsule, including calycosin glucoside, ginsenoside Rg1, ginsenoside Rb1, taurocholic acid sodium, formonetin, and calycosin glucoside. The components of WeiNaiAn capsule promoted the wound healing of the epithelial cell in vitro. Moreover, the components of WeiNaiAn capsule inhibited the protein expressions of phosphoinositide 3-kinase /protein kinase B /mammalian target of rapamycin in hydrogen peroxide or lipopolysaccharides-induced cell model. In conclusion, WeiNaiAn capsule improves intestinal mucosal injury by regulating cell migration, enhancing antioxidant activity, and promoting the structure of the bacterial community homeostasis, the multiple targets provide the parameters for the treatment in the clinic.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"173 ","pages":"Article 106609"},"PeriodicalIF":3.4,"publicationDate":"2024-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141332399","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":"Novel meroterpene-like compounds inhibit ferroptosis through Fe2+ chelation","authors":"Shiyang Lou ,&nbsp;Yan-Xiang Liu ,&nbsp;Chao Xia ,&nbsp;Qiang Zhang ,&nbsp;Lu Deng ,&nbsp;Jiang-Jiang Tang","doi":"10.1016/j.biocel.2024.106610","DOIUrl":"https://doi.org/10.1016/j.biocel.2024.106610","url":null,"abstract":"<div><p>Colorectal cancer (CRC) is the third most common type of cancer in the world. It is characterized by complex crosstalk between various signaling pathways, as a result of which it is highly challenging to identify optimal therapeutic targets and design treatment strategies. In this study, we tested the effect of 700 compounds on the CRC cell line HT-29 by using the sulforhodamine B assay and screened out 17 compounds that exhibited high toxicity (indicated by an inhibition rate of ≥75 % when applied at a concentration of 10 µM) against the HT-29 cell line. Next, we investigated the mechanisms underlying the effects of these 17 highly toxic compounds. The results of ferroptosis analysis and electron microscopy showed that compounds 575 and 578 were able to significantly reverse RSL3-induced increase in ferroptosis, while compound 580 had a less pronounced ferroptosis-regulating effect. In subsequent experiments, western blotting showed that compounds 575, 578, and 580, which belong to a class of meroterpene-like compounds that affect ferroptosis, do not induce autophagy or apoptosis in the CRC cell line. Instead, Fe²⁺ chelation experiments showed that these three compounds can serve as iron chelators by chelating Fe²⁺ at a 1:1 (chelator: Fe²⁺) ratio. Specifically, the aldehyde and hydroxyl groups of the benzene ring in these compounds may chelate Fe²⁺, thus reducing Fe²⁺ levels in cells and inhibiting ferroptosis. These results indicate that these novel meroterpene-like compounds are potential therapeutic small-molecule candidates for targeting ferroptosis in tumors.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"173 ","pages":"Article 106610"},"PeriodicalIF":4.0,"publicationDate":"2024-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141325280","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":"Mutations in the SLC35C1 gene, contributing to significant differences in fucosylation patterns, may underlie the diverse phenotypic manifestations observed in leukocyte adhesion deficiency type II patients","authors":"E. Skurska ,&nbsp;B. Szulc ,&nbsp;K. Kreczko,&nbsp;M. Olczak","doi":"10.1016/j.biocel.2024.106602","DOIUrl":"10.1016/j.biocel.2024.106602","url":null,"abstract":"<div><p>Congenital disorders of glycosylation (CDG) are a large family of genetic diseases resulting from defects in the synthesis of glycans and the attachment of glycans to macromolecules. The CDG known as leukocyte adhesion deficiency II (LAD II) is an autosomal, recessive disorder caused by mutations in the <em>SLC35C1</em> gene, encoding a transmembrane protein of the Golgi apparatus, involved in GDP-fucose transport from the cytosol to the Golgi lumen. In this study, a cell-based model was used as a tool to characterize the molecular background of a therapy based on a fucose-supplemented diet. Such therapies have been successfully introduced in some (but not all) known cases of LAD II. In this study, the effect of external fucose was analyzed in SLC35C1 KO cell lines, expressing 11 mutated SLC35C1 proteins, previously discovered in patients with an LAD II diagnosis. For many of them, the <em>cis</em>-Golgi subcellular localization was affected; however, some proteins were localized properly. Additionally, although mutated SLC35C1 caused different α-1–6 core fucosylation of N-glycans, which explains previously described, more or less severe disorder symptoms, the differences practically disappeared after external fucose supplementation, with fucosylation restored to the level observed in healthy cells. This indicates that additional fucose in the diet should improve the condition of all patients. Thus, for patients diagnosed with LAD II we advocate careful analysis of particular mutations using the SLC35C1-KO cell line-based model, to predict changes in localization and fucosylation rate. We also recommend searching for additional mutations in the human genome of LAD II patients, when fucose supplementation does not influence patients’ state.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"173 ","pages":"Article 106602"},"PeriodicalIF":4.0,"publicationDate":"2024-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141285200","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}