International Journal of Biochemistry & Cell Biology最新文献

{"title":"The role of nicotinic acetylcholine receptors in the pathophysiology and pharmacotherapy of autism spectrum disorder: Focus on α7 nicotinic receptors","authors":"Murat Oz ,&nbsp;Lina Al Kury ,&nbsp;Bassem Sadek ,&nbsp;Mohamed Omer Mahgoub","doi":"10.1016/j.biocel.2024.106634","DOIUrl":"10.1016/j.biocel.2024.106634","url":null,"abstract":"<div><p>Postmortem studies have revealed that brains of individuals with autism spectrum disorder (ASD) exhibit abnormalities in various components of the cholinergic system including cholinergic receptors, projections, and nuclei. Deletions in the 15q13.3 region which encompasses <em>CHRNA7,</em> the gene that encodes the α7-nACh receptor, have been linked to various neurodevelopmental disorders, including ASD. In addition, the involvement of α7-nACh receptors in biological phenomena known to play a role in the pathophysiology of ASD such as cognitive functions, learning, memory, neuroinflammation, and oxidative stress, as well as the excitation-inhibition balance in neuronal circuits and maternal immune activation have been reported in previous studies. Furthermore, evolving preclinical and clinical literature supports the potential therapeutic benefits of using selectively acting cholinergic compounds, particularly those targeting the α7-nACh receptor subtype, in the treatment of ASD. This study reviews the previous literature on the involvement of nACh receptors in the pathophysiology of ASD and focuses on the α7-nACh receptor as a potential therapeutic target.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"174 ","pages":"Article 106634"},"PeriodicalIF":3.4,"publicationDate":"2024-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141879698","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":"Corrigendum to “Graphene oxide leads to mitochondrial-dependent apoptosis by activating ROS-p53-mPTP pathway in intestinal cells” [Int. J. Biochem. Cell Biol. 146 (2022) 106206]","authors":"Weiyu Feng,&nbsp;Jinbang Wang,&nbsp;Baodong Li,&nbsp;Yonggang Liu,&nbsp;Dongli Xu,&nbsp;Ke Cheng,&nbsp;Jing Zhuang","doi":"10.1016/j.biocel.2024.106633","DOIUrl":"10.1016/j.biocel.2024.106633","url":null,"abstract":"","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"174 ","pages":"Article 106633"},"PeriodicalIF":3.4,"publicationDate":"2024-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1357272524001250/pdfft?md5=bfb2c0e607dd351ef578abab05fc12f8&pid=1-s2.0-S1357272524001250-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141762322","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":"Iron metabolism in doxorubicin-induced cardiotoxicity: From mechanisms to therapies","authors":"Hua Ye ,&nbsp;Lin Wu ,&nbsp;Yanmei Liu","doi":"10.1016/j.biocel.2024.106632","DOIUrl":"10.1016/j.biocel.2024.106632","url":null,"abstract":"<div><p>Doxorubicin (DOX) is an anti-tumor agent for chemotherapy, but its use is often hindered by the severe and life-threatening side effect of cardiovascular toxicity. In recent years, studies have focused on dysregulated iron metabolism and ferroptosis, a unique type of cell death induced by iron overload, as key players driving the development of DOX-induced cardiotoxicity (DIC). Recent advances have demonstrated that DOX disturbs normal cellular iron metabolism, resulting in excessive iron accumulation and ferroptosis in cardiomyocytes. This review will explore how dysregulated iron homeostasis and ferroptosis drive the progression of DIC. We will also discuss the current approaches to target iron metabolism and ferroptosis to mitigate DIC. Besides, we will discuss the limitations and challenges for clinical translation for these therapeutic regimens.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"174 ","pages":"Article 106632"},"PeriodicalIF":3.4,"publicationDate":"2024-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141762323","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":"NS8593 inhibits chondrocyte ferroptosis and alleviates cartilage injury in rat adjuvant arthritis through TRPM7 / HO-1 pathway","authors":"Wenjuan Hao ,&nbsp;Rendi Zhu ,&nbsp;Hailin Zhang ,&nbsp;Yong Chen ,&nbsp;Shufang Li ,&nbsp;Fuli Zhou ,&nbsp;Wei Hu ,&nbsp;Renpeng Zhou","doi":"10.1016/j.biocel.2024.106618","DOIUrl":"10.1016/j.biocel.2024.106618","url":null,"abstract":"<div><p>Ferroptosis is an emerging target in rheumatoid arthritis (RA). We previously reported that transient receptor potential melastatin 7 (TRPM7) expression is correlated with RA cartilage destruction and demonstrated that TRPM7 mediates ferroptosis in chondrocytes. Here, we further determined the role and mechanism of (R)-N-(Benzimidazol-2-yl)-1,2,3,4-tetrahydro-1-naphthylamine (NS8593), a TRPM7 inhibitor, in chondrocyte ferroptosis of RA. We established <em>in vitro</em> models of ferroptosis in human chondrocytes (C28/I2 cells) by using ferroptosis inducer Erastin. The results showed that NS8593 could protect C28/I2 cells from ferroptosis by inhibiting TRPM7 channel, which was manifested by restoring cell viability, reducing cytotoxicity, affecting the expression of ferroptosis marker protein, and restoring redox balance to alleviate Erastin-induced oxidative stress injury. Mechanistically, the Heme oxygenase-1 (HO-1) axis responded to Erastin stimulation, which resulted in TRPM7-mediated chondrocyte ferroptosis, NS8593 could reduce the expression of HO-1 by inhibiting TRPM7 channel. Moreover, NS8593 alleviated articular cartilage destruction and inhibited chondrocyte ferroptosis in AA rats. In conclusion, NS8593 mitigated articular cartilage damage and chondrocyte ferroptosis through the TRPM7/HO-1 pathway, suggesting that NS8593 may be a potential novel drug for the treatment of RA.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"174 ","pages":"Article 106618"},"PeriodicalIF":3.4,"publicationDate":"2024-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141762324","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":"Upregulation of peroxisome proliferator-activated receptor γ with resorcinol alleviates reactive oxygen species generation and lipid accumulation in neuropathic lysosomal storage diseases","authors":"Hyungkuen Kim,&nbsp;Sung-Jo Kim","doi":"10.1016/j.biocel.2024.106631","DOIUrl":"10.1016/j.biocel.2024.106631","url":null,"abstract":"<div><p>Neuropathic lysosomal storage diseases (NLSDs), including ceroid lipofuscinosis neuronal 3 (CLN3) disease and Gaucher disease type 2 (GD2), are typically present in adolescents; however, there are no approved therapies. CLN3 disease is the most common of the 13 types of neuronal ceroid lipofuscinosis, and Gaucher disease is the most common type of lysosomal storage disease. These NLSDs share oxidative stress and lysosomal dysfunction with Parkinson’s disease. In this study, we used patient-derived cells (PDCs) and resorcinol to develop a therapeutic agent based on peroxisome proliferator-activated receptor γ (PPARγ) activation. PPARγ is a major regulator of autophagy and reactive oxygen species (ROS). Resorcinol, a polyphenolic compound, has been reported to exhibit PPARγ agonistic potential. Protein levels were analyzed by immunoblotting and immunofluorescence microscopy. Changes in cellular metabolism, including ROS levels, lipid droplet content, and lysosomal activity, were measured by flow cytometry. Resorcinol reduced ROS levels by suppressing hypoxia-inducible factor 1α levels in CLN3-PDCs. Resorcinol upregulated autophagy and reduced lipid accumulation in CLN3-PDCs; however, these effects were abolished by autophagy inhibitors. Resorcinol increased nuclear PPARγ levels in CLN3-PDCs, and PPARγ antagonists abolished the therapeutic effects of resorcinol. Moreover, Resorcinol upregulated nuclear PPARγ levels and lysosomal activity in GD2-PDCs, and reduced lipid accumulation and ROS levels. In summary, resorcinol alleviated the shared pathogenesis of CLN3 disease and GD2 through PPARγ upregulation. These findings suggest that resorcinol is a potential therapeutic candidate for alleviating NLSD progression.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"174 ","pages":"Article 106631"},"PeriodicalIF":3.4,"publicationDate":"2024-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141736495","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 \"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,&nbsp;Lei Pei,&nbsp;Danhua Zhang,&nbsp;Feng Xu,&nbsp;Enxiang Zhou,&nbsp;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 ,&nbsp;Luigi Mita ,&nbsp;Marco Miceli ,&nbsp;Antonella Doto ,&nbsp;Angela Nebbioso ,&nbsp;Floriana De Bellis ,&nbsp;Mariarosaria Conte ,&nbsp;Annunziata Minichiello ,&nbsp;Fabio Manzo ,&nbsp;Vincenzo Carafa ,&nbsp;Adriana Basile ,&nbsp;Daniela Rigano ,&nbsp;Sergio Sorbo ,&nbsp;Rosa Castaldo Cobianchi ,&nbsp;Ettore Mariano Schiavone ,&nbsp;Felicetto Ferrara ,&nbsp;Mariacarla De Simone ,&nbsp;MariaTeresa Vietri ,&nbsp;Michele Cioffi ,&nbsp;Vincenzo Sica ,&nbsp;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}