International Journal of Biochemistry & Cell Biology最新文献

{"title":"Corrigendum to \"Dimerization of ZIP promotes its transcriptional repressive function and biological activity\" [Int. J. Biochem. Cell Biol. 44 (2012) 886-895].","authors":"Bin Gui, Xiao Han, Yu Zhang, Jing Liang, Dandan Wang, Chenghao Xuan, Zhipeng Yu, Yongfeng Shang","doi":"10.1016/j.biocel.2024.106715","DOIUrl":"https://doi.org/10.1016/j.biocel.2024.106715","url":null,"abstract":"","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":" ","pages":"106715"},"PeriodicalIF":3.4,"publicationDate":"2024-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142796476","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":"Prevention of fenitrothion induced hepatic toxicity by saponarin via modulating TLR4/MYD88, JAK1/STAT3 and NF-κB signaling pathways.","authors":"Hesham M Hassan, Mahmoud El Safadi, Muhammad Faisal Hayat, Ahmed Al-Emam","doi":"10.1016/j.biocel.2024.106716","DOIUrl":"https://doi.org/10.1016/j.biocel.2024.106716","url":null,"abstract":"<p><p>Fenitrothion (FEN) is an organophosphate insecticidal agent that is considered as major source of organs toxicity. Saponarin (SAP) is a naturally occurring novel flavone that exhibits immense medicinal properties. The current trial was executed to evaluate the treatment potential of SAP against FEN instigated liver toxicity. Thirty-two male albino rats (Rattus norvegicus) were apportioned into four groups including control, FEN (10mg/kg), FEN (10mg/kg) + SAP (80mg/kg), and SAP (80mg/kg) alone treated group. It was revealed that FEN administration upregulated the gene expression of TNF-α, TLR4, IL-1β, MYD88, IL-6, TRAF6, COX-2, NF-κB, JAK1 and STAT3 while suppressing the gene expression of IκB. Moreover, the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) were promoted while the activities of catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), heme-oxygenase-1 (HO-1) and glutathione reductase (GSR) were suppressed after FEN provision. Furthermore, FEN administration notably escalated the concentrations of hepatic enzymes including alanine transaminase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT) and alkaline phosphatase (ALP) whereas reduced the concentrations of total proteins and albumin. Besides, FEN intake upregulated the levels of Caspase-9, Bax and Caspase-3 while diminishing the levels of Bcl-2. Hepatic histology was distorted after FEN provision. Nonetheless, SAP treatment remarkably protected the normal state of liver via regulating abovementioned irregularities. Our in-silico calculations confirm that SAP hold that potential to interact with binding pocket of these proteins, highlighting its ability as a therapeutic compound to alleviate FEN-induced liver damage.</p>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":" ","pages":"106716"},"PeriodicalIF":3.4,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142792454","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":"5'tiRNA-33-CysACA-1 promotes septic cardiomyopathy by targeting PGC-1α-mediated mitochondrial biogenesis.","authors":"Ludong Yuan, Jing Li, Leijing Yin, Xiaofang Lin, Dan Ni, Chuanhuan Deng, Pengfei Liang, Bimei Jiang","doi":"10.1016/j.biocel.2024.106714","DOIUrl":"https://doi.org/10.1016/j.biocel.2024.106714","url":null,"abstract":"<p><strong>Background: </strong>We revealed for the first time that the expression of 158 tRNA-derived small RNAs (tsRNAs) was altered in septic cardiomyopathy (SCM) by microarray analysis, and we selected 5'tiRNA-33-CysACA-1, which was the most significantly up-regulated, as a representative to explore the roles and mechanisms of tsRNAs in SCM.</p><p><strong>Methods: </strong>We constructed a sepsis model by cecum ligation and puncture (CLP) in mice and detected the expression of 5'tiRNA-33-CysACA-1 using quantitative real-time PCR (qRT-PCR). The supernatant generated after LPS stimulation of macrophages was used as the conditional medium (CM) to stimulate H9C2 and established the injured cell model. CCK-8 and LDH release assays were used to detect cell viability and cell death. Mitochondrial membrane potential (MMP), ATP production, ROS production, and Mitotracker Red mitochondrial morphology were assayed to assess mitochondrial function. Expression of mRNA for molecules related to the mitochondrial quality control system was verified by qRT-PCR. The mechanism by which 5'tiRNA-33-CysACA-1 regulates peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) expression was examined by western blot, mRNA stability analysis, and rescue experiments.</p><p><strong>Results: </strong>Expression of 5'tiRNA-33-CysACA-1 was elevated in cardiac tissue and H9C2 cells during septic myocardial injury. Stimulation of the CM resulted in cardiomyocyte injury and impaired mitochondrial function. Transfection of 5'tiRNA-33-CysACA-1 mimic in CM further downregulated PGC-1α expression, inhibited mitochondrial biogenesis thereby impairing mitochondrial function and leading to decreased cardiomyocyte activity and increased cell death. In contrast, transfection of the inhibitor ameliorated the above biological processes. In addition, mRNA stability assay and bioinformatics analysis showed that 5'tiRNA-33-CysACA-1 led to a decrease in the stability of PGC-1α mRNA, which in turn downregulated the expression of PGC-1α and promoted the development of SCM.</p><p><strong>Conclusions: </strong>5'tiRNA-33-CysACA-1 expression is upregulated in SCM and inhibits mitochondrial biogenesis by targeting PGC-1α and decreasing the stability of PGC-1α mRNA, leading to mitochondrial dysfunction and promoting the development of SCM.</p>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":" ","pages":"106714"},"PeriodicalIF":3.4,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142781714","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":"Adipose tissue macrophages-derived exosomal MiR-500a-5p under high glucose promotes adipocytes inflammation by suppressing Nrf2 expression","authors":"Yong-Zhen Li ,&nbsp;Yuan Tian ,&nbsp;Chen Yang ,&nbsp;Yi-Fan Liu ,&nbsp;Shun-Lin Qu ,&nbsp;Liang Huang ,&nbsp;Chi Zhang","doi":"10.1016/j.biocel.2024.106713","DOIUrl":"10.1016/j.biocel.2024.106713","url":null,"abstract":"<div><h3>Background</h3><div>Type 2 diabetes (T2DM) is a chronic metabolic disorder characterized by insulin resistance and chronic inflammation. Adipose tissue macrophages (ATMs), central players in mediating pro-inflammatory responses within adipose tissue, have been shown to influence insulin sensitivity through exosome secretion. While the role of macrophages-derived exosomal miRNA has been studied in various diseases, their pathogenic roles in T2DM, particularly ATMs-derived exosomal miRNA in adipose tissue inflammation, remain underexplored.</div></div><div><h3>Objectives</h3><div>This study focuses specifically on T2DM, investigating the role of ATM-derived exosomal miRNAs in adipose tissue inflammation, a critical factor in the pathogenesis of T2DM.</div></div><div><h3>Methods</h3><div>ATM were isolated from visceral adipose tissues in patients with or without diabetes. Differentially expressed miRNAs in ATM-derived exosomes were predicted by high-throughput RNA sequencing. The RAW264.7 macrophages and 3T3-L1 preadipocytes was selected as a model system. Quantitative RT-PCR was used to assess miR-500a-5p expression. The direct binding of miR-500a-5p to Nrf2 mRNA 3′ UTR was verified by dual luciferase assay.</div></div><div><h3>Results</h3><div>MiR-500a-5p was also enriched in the exosomes of high-glucose-treated macrophages. Furthermore, these exosomes induced high expression of miR-500a-5p and activation of the NLRP3 inflammasome in adipocytes when co-cultured with them. Additionally, the reduction of miR-500a-5p expression in macrophages by using a miR-500a-5p inhibitor ameliorated the pro-inflammatory properties of the exosomes, and co-culturing these exosomes with adipocytes resulted in decreased expression of NLRP3 inflammasome-associated proteins in adipocytes. In contrast, induction of miR-500a-5p expression led to the opposite results. Moreover, the dual-luciferase assay confirmed that miR-500a-5p directly targeted the 3′ UTR of Nrf2 mRNA. Unlike miR-500a-5p, Nrf2 exhibited an anti-inflammatory response.</div></div><div><h3>Conclusion</h3><div>The results indicate that ATM-derived exosomal miR-500a-5p promotes NLRP3 inflammasome activation and adipose tissue inflammation through down-regulation of Nrf2 in adipocytes.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"178 ","pages":"Article 106713"},"PeriodicalIF":3.4,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142756791","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":"The potential regulation of the miR-17–92a cluster by miR-21","authors":"Meredith Hill ,&nbsp;Sarah Stapleton ,&nbsp;Phuong Thao Nguyen ,&nbsp;Dayna Sais ,&nbsp;Fiona Deutsch ,&nbsp;Valerie C. Gay ,&nbsp;Deborah J. Marsh ,&nbsp;Nham Tran","doi":"10.1016/j.biocel.2024.106705","DOIUrl":"10.1016/j.biocel.2024.106705","url":null,"abstract":"<div><div>MicroRNAs (miRNA,miRs) are small noncoding RNAs that are ubiquitously expressed in all mammalian cells. Their primary function is the regulation of nascent RNA transcripts by direct binding to regions on the target. There is now exciting data to suggest that these miRNAs can bind to other miRNAs, and this may have a broader impact on gene regulation in disease states. The oncomiR miR-21 is one of the highest-expressing miRNAs in cancer cells, and in this study, we characterise which miRNAs could be potential targets of miR-21. In cancer cells delivered with a miR-21 mimic, there was an observable shift of the miRNA milieu. We demonstrate that the miR-17–92a cluster, which harbours six miRNA members, may be a target for miR-21 regulation. Additionally, the primary transcript of miR-17–92a was reduced in the presence of miR-21. In the broader context of miR:miR regulation, overexpression of miR-21 shifted the expression of more than 150 miRNAs, including those known to regulate genes in cancer pathways such as the MAPK signalling and FoxO pathways. This study expands upon our limited understanding of miR:miR regulatory network and reinforces the concept that miRNAs can regulate each other, thereby influencing broader gene networks.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"178 ","pages":"Article 106705"},"PeriodicalIF":3.4,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142756790","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":"Unveiling a novel signalling pathway involving NRF2 and PGAM5 in regulating the mitochondrial unfolded protein response in stressed cardiomyocytes","authors":"Rahme Nese Safakli ,&nbsp;Stephen Gray ,&nbsp;Nadia Bernardi ,&nbsp;Ioannis Smyrnias","doi":"10.1016/j.biocel.2024.106704","DOIUrl":"10.1016/j.biocel.2024.106704","url":null,"abstract":"<div><div>The mitochondrial unfolded protein response (UPRmt) is a conserved signalling pathway that initiates a specific transcriptional programme to maintain mitochondrial and cellular homeostasis under stress. Previous studies have demonstrated that UPRmt activation has protective effects in the pressure-overloaded human heart, suggesting that robust UPRmt stimulation could serve as an intervention strategy for cardiovascular diseases. However, the precise mechanisms of UPRmt regulation remain unclear. In this study, we present evidence that the NRF2 transcription factor is involved in UPRmt activation in cardiomyocytes during conditions of mitochondrial stress. Silencing NRF2 partially reduces UPRmt activation, highlighting its essential role in this pathway. However, constitutive activation of NRF2 via inhibition of its cytosolic regulator KEAP1 does not increase levels of UPRmt activation markers, suggesting an alternative regulatory mechanism independent of the canonical KEAP1-NRF2 axis. Further analysis revealed that NRF2 likely affects UPRmt activation through its interaction with PGAM5 at the mitochondrial membrane. Disruption of PGAM5 in cardiomyocytes subjected to mitochondrial stress reduces the interaction between PGAM5 and NRF2, enhancing nuclear translocation of NRF2 and significantly upregulating the UPRmt in an NRF2-dependent manner. This NRF2-regulated UPRmt amplification improves mitochondrial respiration, reflecting an enhanced capacity for cardiomyocytes to meet elevated energetic demands during mitochondrial stress. Our findings highlight the therapeutic potential of targeting the NRF2-PGAM5-KEAP1 signalling complex to amplify the UPRmt in cardiomyocytes for cardiovascular and other diseases associated with mitochondrial dysfunction. Future studies should aim to elucidate the mechanisms via which NRF2 enhances the protective effects of UPRmt, thereby contributing to more targeted therapeutic approaches.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"178 ","pages":"Article 106704"},"PeriodicalIF":3.4,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142752208","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":"Immune-epithelial cell interactions in lung development, homeostasis and disease.","authors":"Masahiro Yoshida, Romina Arzili, Marko Z Nikolić","doi":"10.1016/j.biocel.2024.106703","DOIUrl":"10.1016/j.biocel.2024.106703","url":null,"abstract":"<p><p>The importance of the crosstalk between lung epithelial and immune cells, which emerges from early development and lasts throughout life, is corroborated by a growing body of scientific evidence. This communication not only has a role in driving lung morphogenesis during development, but it is also required in adulthood for the maintenance of homeostasis and repair following infection or injury. Disruption of the intricate immune-epithelial crosstalk can lead to diseases such as COPD and IPF. In this review we summarise the current knowledge regarding the communication between various immune and epithelial cells in development, homeostasis, regeneration and disease, while identifying the current gaps in our knowledge required to facilitate the development of more effective therapies.</p>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":" ","pages":"106703"},"PeriodicalIF":3.4,"publicationDate":"2024-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142734398","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":"Regulatory role of AMPK/Nrf2 signaling pathway in sevoflurane-enhanced intestinal protection against ischemia-reperfusion injury","authors":"Xiaohua Zeng ,&nbsp;Shan Jiang ,&nbsp;Yinghui Wu ,&nbsp;Liang Zhong ,&nbsp;Xin Liu","doi":"10.1016/j.biocel.2024.106702","DOIUrl":"10.1016/j.biocel.2024.106702","url":null,"abstract":"<div><div>Intestinal ischemia-reperfusion (I/R) injury is common in clinical settings and is associated with high mortality. Sevoflurane, a widely used anesthetic, has long recognized for its protective effects against intestinal I/R injury, though the underlying mechanisms remain largely uncharacterized. In this study, using both <em>in vivo</em> and <em>in vitro</em> models, we uncovered a novel role of sevoflurane in preventing ferroptotic cell death during intestinal I/R injury. Sevoflurane treatment activated transcription factor Nrf2 (nuclear factor erythroid 2-related factor 2) and upregulated its target genes involved in iron sequestration (FTL) and glutathione biosynthesis (SLC7A11 and GCLM). These changes reduced intracellular ferrous iron levels and alleviated iron-dependent oxidative stress and lipid peroxidation, a hallmark of ferroptosis. Importantly, through large-scale kinome screening, we revealed that sevoflurane-induced Nrf2 activation was mediated by AMP-activated protein kinase (AMPK). Sevoflurane treatment activated AMPK, which subsequently phosphorylated Nrf2 and prevented its degradation. Stabilized Nrf2 then entered nucleus, where it promoted the transcription of downstream targets. We concluded that sevoflurane exerts anti-ferroptoic function in intestinal I/R through the AMPK/Nrf2 signaling pathway. These results expand our knowledge about the pathogenesis of intestinal I/R injury, and provide novel insights for optimizing clinical treatments and developing novel therapeutic strategies.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"177 ","pages":"Article 106702"},"PeriodicalIF":3.4,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142711848","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":"Antitumor effect of bromo-naphthoquinone associated with tannic acid in triple negative breast cancer cells","authors":"Emanuelle Pangoni de Carvalho ,&nbsp;Adriano de Souza Pessoa ,&nbsp;Flávia Godoy Iano ,&nbsp;Laura Ribeiro ,&nbsp;Bianca Leme ,&nbsp;Luis Francisco Borges ,&nbsp;Mariana Liessa Rovis Sanches ,&nbsp;Valdecir Farias Ximenes ,&nbsp;Rodrigo Cardoso de Oliveira","doi":"10.1016/j.biocel.2024.106697","DOIUrl":"10.1016/j.biocel.2024.106697","url":null,"abstract":"<div><div>Triple-negative breast cancer (TNBC) is an aggressive type of tumor that tends to recur in women. It is characterized by the absence of hormonal receptors, making it challenging to diagnosis and treatment. In this study, we investigated the anti-tumor effects of a pro-oxidant naphthoquinone derivative called bromo-naphthoquinone (BrNQ) isolated and combined with the antioxidant tannic acid (TA) in order to improve treatment. We used tumor cell lines MDA-MB-231 and HCC-70, as well as normal breast cells, HB4a, as control. Initially, viability assays conducted within 72 hours showed that the combination of compounds had a synergistic and notable cytotoxic effect on the tumor cells. The increased cytotoxicity appeared to be linked to changes in the cellular redox status, as indicated by a significant rise in reactive oxygen species (ROS) and though alterations in the level of thiol. The treatment also induced apoptosis, inhibited proliferation, and reduced migration, particularly in the MDA-MB-231 cell line. Furthermore, relevant changes were detected in the expression of Bcl-2, BAX, FAS, and BIRC-5, while no significant alteration in the expression of NOXs was observed. In conclusion, our findings suggested that the combination of BrNQ and TA though the ability to change redox status in tumor cells could act as a potential adjuvant treatment modality for improve prognosis in TNBC.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"177 ","pages":"Article 106697"},"PeriodicalIF":3.4,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142683277","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":"Use of Myriocin as co-adjuvant in glaucoma surgery: An in vitro study","authors":"Linda Montavoci ,&nbsp;Dario Romano ,&nbsp;Leonardo Colombo ,&nbsp;Aida Zulueta ,&nbsp;Michele Dei Cas ,&nbsp;Mariangela Scavone ,&nbsp;Delfina Tosi ,&nbsp;Clara Bernardelli ,&nbsp;Alessandro Autelitano ,&nbsp;Marco Trinchera ,&nbsp;Luca Rossetti ,&nbsp;Anna Caretti","doi":"10.1016/j.biocel.2024.106699","DOIUrl":"10.1016/j.biocel.2024.106699","url":null,"abstract":"<div><div>Mitomycin C as well as other antiproliferative drugs are off-label agents widely used to prevent the failure of glaucoma surgery due to activation of Tenon’s fibroblasts and the ensuing excessive subconjunctival scarring. Though efficacious, these treatments are associated with some severe long-term complications, so it is crucial to investigate less cytotoxic compounds as adjuvant therapy in glaucoma surgery. The aim of this study was to evaluate the effect and potential cytotoxicity of Myriocin, a natural sphingolipid synthesis inhibitor, on TGF-β1-induced myofibroblasts transformation of human dermal fibroblasts. We found that myriocin significantly attenuated the transcript levels of αSMA, CTGF, and MMP9 which are involved in the fibrosis process. Mitomycin C poorly affects the same pro-fibrotic markers while reducing fibroblasts motility as much as myriocin. At similar doses, five minutes of mitomycin C treatment consistently affects human dermal fibroblast viability and proliferation compared to prolonged myriocin application, strengthening already published data on the good tolerability of this natural compound. Our results draw attention to the use of myriocin as an adjuvant in glaucoma surgery due to the effectiveness in reducing fibroblasts to myofibroblasts transformation and the low cytotoxicity.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"177 ","pages":"Article 106699"},"PeriodicalIF":3.4,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142689403","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}