Biology Direct最新文献

{"title":"Exosomes containing circSCP2 in colorectal cancer promote metastasis via sponging miR-92a-1-5p and interacting with PTBP1 to stabilize IGF2BP1.","authors":"Qing Meng, Haoyi Xiang, Yijing Wang, Kepeng Hu, Xin Luo, Jiawei Wang, Engeng Chen, Wei Zhang, Jiaxin Chen, Xiaoyu Chen, Huogang Wang, Zhenyu Ju, Zhangfa Song","doi":"10.1186/s13062-024-00571-1","DOIUrl":"10.1186/s13062-024-00571-1","url":null,"abstract":"<p><p>Exosomes have emerged as significant biomarkers for multiple diseases, including cancers. Circular RNAs (circRNAs), abundant in exosomes, are involved in regulating cancer development. However, the regulatory function and the underlying molecular mechanism of hsa_circ_0006906 (circSCP2) in colorectal cancer (CRC) metastasis remain unclear. A competing endogenous RNA microarray was used to analyze circRNA expression in serum exosomes in patients with CRC at early and late stages. circSCP2 expression was evaluated using qRT-PCR. The biological functions of circSCP2 in CRC were assessed through in vitro and in vivo experiments. The molecular mechanism of circSCP2 was explored using western blotting, RNA pulldown, RNA immunoprecipitation, luciferase assays, and relative rescue experiments. circSCP2 expression was significantly elevated in CRC tissues, with higher levels in serum exosomes correlating with advanced TNM stages. circSCP2 knockdown inhibited CRC cell proliferation, migration, invasion, and metastasis in vitro and in vivo. Mechanistically, circSCP2 sponged miR-92a-1-5p to increase insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) expression. Additionally, circSCP2 directly bound to and stabilized polypyrimidine tract binding protein 1 (PTBP1) by inhibiting protein ubiquitination, resulting in IGF2BP1 mRNA stabilization and enhanced CRC migration and invasion. Our findings demonstrate that circSCP2 regulates the miR-92a-1-5p/IGF2BP1 pathway, promotes PTBP1/IGF2BP1 interaction, and accelerates CRC progression. Exosomal circSCP2 is a promising circulating biomarker for CRC prognosis and needs further therapeutic investigation.</p>","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":"19 1","pages":"130"},"PeriodicalIF":5.7,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11661319/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Valentina Tassinari, the legacy of a young scientist.","authors":"Gerry Melino, Eleonora Candi, Daniele Marcoccia","doi":"10.1186/s13062-024-00585-9","DOIUrl":"10.1186/s13062-024-00585-9","url":null,"abstract":"","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":"19 1","pages":"140"},"PeriodicalIF":5.7,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11660705/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrative in-silico and in-vitro analysis of taurine and vitamin B12 in modulating PPARγ and Wnt signaling in hyperhomocysteinemia-induced osteoporosis.","authors":"Mazumder Adhish, I Manjubala","doi":"10.1186/s13062-024-00581-z","DOIUrl":"10.1186/s13062-024-00581-z","url":null,"abstract":"<p><p>Peroxisome proliferator-activated receptor-γ (PPARγ) is a critical regulator of adipogenesis and bone metabolism, playing complex roles in osteoporosis. This study investigates the effects of taurine and homocysteine on PPARγ, focusing on their roles in osteoclastogenesis and bone health. In-silico analyses, including molecular docking and molecular dynamic simulations, revealed that both taurine and homocysteine bind competitively to the PPARγ ligand-binding domain, exhibiting distinctive antagonistic modes, including destabilization of PPARγ's key helices H3, H4/5, H11, and H12. In-vitro experiments further supported these results, demonstrating that taurine protects against oxidative damage, enhances bone mineralization, and reduces the expression levels of PPARγ, while also downregulating negative regulators of the Wnt signaling pathway, such as SOST and DKK1. Homocysteine, on the other hand, was observed to increase the expression of these regulators and impair bone formation. Vitamin B12 was included in the study due to its known role in mitigating hyperhomocysteinemia, a condition linked to impaired bone health and reduced taurine levels. While vitamin B12 alone demonstrated some beneficial effects, it did not achieve the same level of efficacy as taurine. However, a combination of taurine and vitamin B12 showed greater efficacy in ameliorating hyperhomocysteinemia-induced osteoporosis. Overall, this study highlights taurine's therapeutic potential in counteracting the adverse effects of hyperhomocysteinemia on bone health and underscores the need for further research into taurine's mechanisms in osteoporosis treatment.</p>","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":"19 1","pages":"141"},"PeriodicalIF":5.7,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11662456/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142871345","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The RRP9-JUN axis promotes breast cancer progression via the AKT signalling pathway.","authors":"Jinliang Huan, Xiaojun Liu, Na Wang, Yuxin Mu, Ling Li, Yiqun Du","doi":"10.1186/s13062-024-00578-8","DOIUrl":"10.1186/s13062-024-00578-8","url":null,"abstract":"<p><strong>Background: </strong>Ribosomal RNA processing 9 (RRP9) is a specific component of the U3 small nucleolar ribonucleoprotein (U3 snoRNP), which is involved in physiological processes and pathological disorders. The purpose of the current study was to investigate the biological roles of RRP9 in breast cancer (BC) progression.</p><p><strong>Methods: </strong>The expression levels of RRP9 in human BC were assessed by immunohistochemical (IHC) staining, qPCR assay and Western blot. Cells were transfected with shRNA plasmids to regulate RRP9 expression. The functional roles were explored by Celigo cell counting assay, colony formation assay, flow cytometry and Transwell assays, as well as construction of Xenograft tumor model. Furthermore, interaction between RRP9 and JUN was determined by Co-immunoprecipitation (Co-IP) assay, protein stability assay, and ubiquitination assay.</p><p><strong>Results: </strong>RRP9 expression was substantially upregulated in BC tissues and was positively associated with lymph node metastasis and poor prognosis. Functional experiments indicated that RRP9 depletion inhibited BC progression both in vitro and in vivo. Using a prime-view human gene expression array and IPA, JUN was identified as a potential downstream target of RRP9. Mechanistically, RRP9 interacted with the JUN protein, and RRP9 deletion decreased JUN protein stability by accelerating JUN ubiquitination and led to JUN degradation via MDM2. Moreover, the regulatory effects of RRP9 on BC cell phenotypes were attenuated by JUN knockdown or the AKT signalling pathway activator SC79.</p><p><strong>Conclusions: </strong>In conclusion, this study revealed the crucial role of RRP9 in BC progression and its probable novel mechanism, suggesting that RRP9 may be a promising candidate for the treatment of BC.</p>","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":"19 1","pages":"131"},"PeriodicalIF":5.7,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11660783/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863262","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Construction of a prognostic model based on disulfidptosis-related genes and identification of CCNA2 as a novel biomarker for hepatocellular carcinoma.","authors":"Tao Wang, Wenxuan Li, Yuelan Wu, Liping You, Chao Zheng, Jinghao Zhang, Lihong Qu, Xuehua Sun","doi":"10.1186/s13062-024-00569-9","DOIUrl":"10.1186/s13062-024-00569-9","url":null,"abstract":"<p><strong>Background: </strong>Disulfidptosis, identified as an innovative form of cellular death subsequent to cuproptosis, is currently under investigation for its mechanisms in oncological contexts. In-depth analyses exploring the relationship between disulfidptosis-related genes (DRGs) and hepatocellular carcinoma (HCC) are currently limited.</p><p><strong>Methods: </strong>Transcriptomic data and clinical information were retrieved from the TCGA and GEO databases (GSE76427 and GSE54236), concentrating on the expression levels of 24 DRGs. Subsequently, multifactor and LASSO regression analyses were utilized to construct the 5-DRG prognostic signature. Immunohistochemistry (IHC) was employed to assess Cyclin A2 (CCNA2) protein expression levels. Quantitative real-time PCR (qRT-PCR) and western blot analyses were conducted to detect transcriptomic and protein expression of CCNA2-targeting short interfering RNA (siRNA). The Cell Counting Kit-8 (CCK-8) assay, EdU staining, and scratch experiments were employed to observe the proliferation and migration of hepatoma cell lines subsequent to CCNA2 inhibition.</p><p><strong>Results: </strong>Three HCC patterns were identified, among which pattern B exhibited the the most unfavorable survival outcomes. Five DRGs (STC2, PBK, CCNA2, SERPINE1, and SLC6A1) were involved to establish the 5-DRG prognostic signature. High-risk groups (HRGs) exhibited prolonged survival durations in comparison to low-risk groups (LRGs). Both bioinformatics analyses and experimental methodologies corroborated the association of CCNA2 with poor prognosis in HCC patients. Functional studies elucidated that interference with CCNA2 significantly inhibited proliferation and migration, while simultaneously promoting apoptosis in hepatoma cells and resulting in the downregulation of epithelial-mesenchymal transition (EMT)-related protein markers.</p><p><strong>Conclusions: </strong>The 5-DRG prognostic signature is proficient in predicting clinical outcomes, informing therapeutic strategies, and elucidating the characteristics of the immune microenvironment in HCC patients. Furthermore, this study elucidates the potential of CCNA2 as an innovative biomarker for HCC.</p>","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":"19 1","pages":"128"},"PeriodicalIF":5.7,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11656849/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142852838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive pan-cancer analysis indicates UCHL5 as a novel cancer biomarker and promotes cervical cancer progression through the Wnt signaling pathway.","authors":"Lingling Bao, Yuefei Wu, Zhengting Ren, Yi Huang, Yue Jiang, Kailang Li, Xin Xu, Yingquan Ye, Zhongxuan Gui","doi":"10.1186/s13062-024-00588-6","DOIUrl":"10.1186/s13062-024-00588-6","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;UCHL5 was initially recognized as a multifunctional molecule. While recent research has highlighted its involvement in tumor malignant biological behaviors, its specific role in promoting tumor cell apoptosis has drawn particular attention. However, the precise relationship between UCHL5 and various tumor types, as well as its influence within the immune microenvironment, remains unclear.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;The transcriptomic data and clinicopathological parameters across 33 cancer types were obtained from TCGA. Clinical pathological parameters of tumor patients, including gender, age, survival time, and staging, are utilized to evaluate the association between UCHL5 and pan-cancer characteristics. The prognostic significance of UCHL5 was evaluated through Cox analysis and Kaplan-Meier (K-M) methods. Protein expression data for UCHL5 were obtained from The Human Protein Atlas database, and its subcellular localization was further investigated. Additionally, potential correlations between UCHL5 and factors such as tumor-infiltrating immune cells, immunomodulators, microsatellite instability (MSI), and tumor mutation burden (TMB) were explored. The relationship between UCHL5 and immunotherapy efficacy was also assessed in independent cohorts, including IMvigor210, GSE78220, GSE67501, and GSE168204. Finally, the impact of UCHL5 on the malignant biological behavior of cervical cancer cells was investigated through in vitro experiments, along with an exploration of the underlying mechanisms.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;We observed that UCHL5 expression levels were elevated in 11 types of cancer tissues compared to their corresponding normal tissues, while levels were lower in five tumor types. Additionally, UCHL5 expression displayed a significant correlation with tumor stage in BRCA, KIRC, LUAD, and TGCT. Cox and K-M analysis indicated that UCHL5 expression was significantly associated with prognosis in KIRC, KICH, CESC, ACC, and UVM. UCHL5 expression was negatively associated with stromal and immune scores in certain cancers. In terms of immune cell infiltration, UCHL5 expression in UCEC, SKCM, and COAD showed a negative correlation with regulatory T cells (Tregs). Furthermore, UCHL5 was widely associated with three types of immunomodulators. It also demonstrated a significant relationship with MSI and TMB in certain cancers and was connected to the immunotherapy efficacy. Finally, in vitro experiments confirmed that UCHL5 knockout enhances apoptosis in cervical cancer cells and disrupts Wnt/β-catenin signaling.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;Pan-cancer analysis indicates that UCHL5 is dysregulated in various tumor tissues and is closely associated with survival prognosis, the tumor immune microenvironment, and the efficacy of immunotherapy in certain cancer types. UCHL5 shows promise as a predictive biomarker, and its specific regulatory mechanisms across different cancers warrant further invest","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":"19 1","pages":"139"},"PeriodicalIF":5.7,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11660788/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prostatitis, benign prostatic hyperplasia, and prostate cancer: a bidirectional Mendelian randomization study and clinical implications for these patients' populations.","authors":"Yi Wang, Guihua Chen, Deng Li, Dongliang Zhang, Qianwei Xing","doi":"10.1186/s13062-024-00575-x","DOIUrl":"10.1186/s13062-024-00575-x","url":null,"abstract":"<p><strong>Background: </strong>No authoritative books or guidelines are currently available for revealing the interrelationships of prostatitis, benign prostatic hyperplasia (BPH), and prostate cancer (PCa). Moreover, no consensus on this issue has been reached among previously published epidemiological studies or meta-analyses.</p><p><strong>Purpose: </strong>We first took advantage of Mendelian randomization to clarify this issue and provide clinical implications for these patients' populations.</p><p><strong>Methods: </strong>Bidirectional two-sample and mediator Mendelian randomization were applied to explore the causal relationships among prostatitis, BPH, and PCa. Sensitivity analyses, including phenotype scanning, heterogeneity, pleiotropy, leave-one-out analysis, and the Steiger test, were conducted to evaluate the robustness and reliability of our results.</p><p><strong>Results: </strong>Our results revealed the interrelationships among prostatitis, BPH, and PCa via Mendelian randomization, confirming that genetic susceptibility to prostatitis or BPH could lead to increased risks of PCa directly or indirectly (P < 0.05). Moreover, mediator Mendelian randomization revealed four potential mediator pathways, including the prostatitis-BPH-PCa, the BPH-PCa-prostatitis, the PCa-prostatitis-BPH, and the PCa-BPH-prostatitis pathways. Based on these, we also provided clinical implications for prostatitis, BPH, and PCa patients' populations, respectively. Interestingly, a total of three vicious circles were revealed by us, including the prostatitis-BPH circle, the BPH-PCa circle, and the prostatitis-BPH-PCa circle. All of these three vicious circles contributed to the progression of benign prostate diseases to malignant diseases.</p><p><strong>Conclusion: </strong>We successfully clarified the interrelationships among prostatitis, BPH, and PCa, providing clinical implications for these patients' populations. A total of three vicious circles were also revealed by us to provide novel ideas for future drug development and guide clinical decision-making.</p>","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":"19 1","pages":"129"},"PeriodicalIF":5.7,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11658280/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142852839","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An exploration into the diagnostic capabilities of microRNAs for myocardial infarction using machine learning.","authors":"Mehrdad Samadishadlou, Reza Rahbarghazi, Kaveh Kavousi, Farhad Bani","doi":"10.1186/s13062-024-00543-5","DOIUrl":"10.1186/s13062-024-00543-5","url":null,"abstract":"<p><strong>Background: </strong>MicroRNAs (miRNAs) have shown potential as diagnostic biomarkers for myocardial infarction (MI) due to their early dysregulation and stability in circulation after MI. Moreover, they play a crucial role in regulating adaptive and maladaptive responses in cardiovascular diseases, making them attractive targets for potential biomarkers. However, their potential as novel biomarkers for diagnosing cardiovascular diseases requires systematic evaluation.</p><p><strong>Methods: </strong>This study aimed to identify a miRNA biomarker panel for early-stage MI detection using bioinformatics and machine learning (ML) methods. miRNA expression data were obtained for early-stage MI patients and healthy controls from the Gene Expression Omnibus. Separate datasets were allocated for training and independent testing. Differential expression analysis was performed to identify dysregulated miRNAs in the training set. The least absolute shrinkage and selection operator (LASSO) was applied for feature selection to prioritize relevant miRNAs associated with MI. The selected miRNAs were used to develop ML models including support vector machine, Gradient Boosted, XGBoost, and a hard voting ensemble (HVE).</p><p><strong>Results: </strong>Differential expression analysis discovered 99 dysregulated miRNAs in the training set. LASSO feature selection prioritized 21 miRNAs. Ten miRNAs were identified in both the LASSO subset and independent test set. The HVE model trained with the selected miRNAs achieved an accuracy of 0.86 and AUC of 0.83 on the independent test set.</p><p><strong>Conclusions: </strong>An integrated framework for robust miRNA selection from omics data shows promise for developing accurate diagnostic models for early-stage MI detection. The HVE model demonstrated good performance despite differences between training and test datasets.</p>","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":"19 1","pages":"127"},"PeriodicalIF":5.7,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11629498/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrating Circle-Seq with transcriptomics reveals genome-wide characterization of extrachromosomal circular DNA for dilated cardiomyopathy.","authors":"Zhenhao Lin, Fangjie Dai, Bo Li, Yongchao Zhao, Changqian Wang","doi":"10.1186/s13062-024-00556-0","DOIUrl":"10.1186/s13062-024-00556-0","url":null,"abstract":"<p><strong>Background: </strong>Extrachromosomal circular DNAs (eccDNAs) are commonly found in various tumors and play a critical role in promoting oncogenesis. However, little is known about the characteristics and nature of eccDNAs in human heart failure. The aim of this study was to comprehensively analyze eccDNAs in human heart failure caused by dilated cardiomyopathy (DCM) and explore their potential functions.</p><p><strong>Methods: </strong>Circle-Seq and RNA-Seq were performed in cardiac tissue samples obtained from patients with DCM and healthy controls to identify eccDNAs and corresponding genes. Inward PCR, outward PCR and Sanger sequencing were conducted to validate the circular structure of eccDNAs. Bioinformatics was employed to probe the transcriptional activity of eccDNAs and their potential roles in the development of DCM. Ligase assisted minicircle accumulation strategy was used to synthesize a 500 bp circular DNA with a random sequence.</p><p><strong>Results: </strong>EccDNAs originated from all chromosomes, with the majority being less than 1 kb in size and about half containing genes or gene fragments. They were derived from specific repeat elements and primarily mapped to 5'UTR, 3'UTR, and CpG islands. Gene-rich chromosomes 17 and 19 exhibited higher eccDNA enrichment. Sequence motifs flanking eccDNA junction sites displayed frequent nucleotide repeats. The circular structure of eccDNAs were confirmed. Integration of Circle-Seq and RNA-Seq data identified that large eccDNAs can be directly transcribed in non-dividing cardiomyocytes, indicating their potential roles in gene expression. Small circular DNA elicited a stronger cytokine response than linear DNA with the same sequence.</p><p><strong>Conclusions: </strong>Our work provided a detailed profiling of eccDNAs in both healthy and DCM hearts and demonstrated the potential functions of both large and small eccDNAs. These findings enhance the comprehension of the role of eccDNAs in cardiac pathophysiology and establish a theoretical foundation for future investigations on eccDNAs in DCM.</p>","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":"19 1","pages":"125"},"PeriodicalIF":5.7,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11606223/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142754736","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Soft X-ray tomography analysis of mitochondria dynamics in Saccharomyces cerevisiae.","authors":"Wei-Ling Huang, Chang-Lin Chen, Zi-Jing Lin, Chia-Chun Hsieh, Mo Da-Sang Hua, Chih-Chan Cheng, Tzu-Hao Cheng, Lee-Jene Lai, Chuang-Rung Chang","doi":"10.1186/s13062-024-00570-2","DOIUrl":"10.1186/s13062-024-00570-2","url":null,"abstract":"<p><strong>Background: </strong>Mitochondria are highly dynamic organelles that constantly undergo processes of fission and fusion. The changes in mitochondrial dynamics shape the organellar morphology and influence cellular activity regulation. Soft X-ray tomography (SXT) allows for three-dimensional imaging of cellular structures while they remain in their natural, hydrated state, which omits the need for cell fixation and sectioning. Synchrotron facilities globally primarily use flat grids as sample carriers for SXT analysis, focusing on adherent cells. To investigate mitochondrial morphology and structure in hydrated yeast cells using SXT, it is necessary to establish a method that employs the flat grid system for examining cells in suspension.</p><p><strong>Results: </strong>We developed a procedure to adhere suspended yeast cells to a flat grid for SXT analysis. Using this protocol, we obtained images of wild-type yeast cells, strains with mitochondrial dynamics defects, and mutant cells possessing distinctive mitochondria. The SXT images align well with the results from fluorescent microscopy. Optimized organellar visualization was achieved by constructing three-dimensional models of entire yeast cells.</p><p><strong>Conclusions: </strong>In this study, we characterized the mitochondrial network in yeast cells using SXT. The optimized sample preparation procedure was effective for suspended cells like yeast, utilizing a flat grid system to analyze mitochondrial structure through SXT. The findings corresponded with the mitochondrial morphology observed under fluorescence microscopy, both in regular and disrupted dynamic equilibrium. With the acquired image of unique mitochondria in Δhap2 cells, our results revealed that intricate details of organelles, such as mitochondria and vacuoles in yeast cells, can be characterized using SXT. Therefore, this optimized system supports the expanded application of SXT for studying organellar structure and morphology in suspended cells.</p>","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":"19 1","pages":"126"},"PeriodicalIF":5.7,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11607810/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142754737","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}