BMB Reports最新文献_第9页

Distinctive contribution of two additional residues in protein aggregation of Aβ42 and Aβ40 isoforms. Aβ42 和 Aβ40 异构体蛋白质聚集过程中另外两个残基的独特作用。

IF 2.9 3区生物学

BMB Reports Pub Date : 2024-06-01

Dongjoon Im, Tae Su Choi

{"title":"Distinctive contribution of two additional residues in protein aggregation of Aβ42 and Aβ40 isoforms.","authors":"Dongjoon Im, Tae Su Choi","doi":"","DOIUrl":"","url":null,"abstract":"Amyloid-β (Aβ) is one of the amyloidogenic intrinsically disordered proteins (IDPs) that self-assemble to protein aggregates, incurring cell malfunction and cytotoxicity. While Aβ has been known to regulate multiple physiological functions, such as enhancing synaptic functions, aiding in the recovery of the blood-brain barrier/brain injury, and exhibiting tumor suppression/antimicrobial activities, the hydrophobicity of the primary structure promotes pathological aggregations that are closely associated with the onset of Alzheimer's disease (AD). Aβ proteins consist of multiple isoforms with 37-43 amino acid residues that are produced by the cleavage of amyloid-β precursor protein (APP). The hydrolytic products of APP are secreted to the extracellular regions of neuronal cells. Aβ 1-42 (Aβ42) and Aβ 1-40 (Aβ40) are dominant isoforms whose significance in AD pathogenesis has been highlighted in numerous studies to understand the molecular mechanism and develop AD diagnosis and therapeutic strategies. In this review, we focus on the differences between Aβ42 and Aβ40 in the molecular mechanism of amyloid aggregations mediated by the two additional residues (Ile41 and Ala42) of Aβ42. The current comprehension of Aβ42 and Aβ40 in AD progression is outlined, together with the structural features of Aβ42/Aβ40 amyloid fibrils, and the aggregation mechanisms of Aβ42/Aβ40. Furthermore, the impact of the heterogeneous distribution of Aβ isoforms during amyloid aggregations is discussed in the system mimicking the coexistence of Aβ42 and Aβ40 in human cerebrospinal fluid (CSF) and plasma. [BMB Reports 2024; 57(6): 263-272].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"263-272"},"PeriodicalIF":2.9,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11214890/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141247443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Tumor antigen PRAME is a potential therapeutic target of p53 activation in melanoma cells. 肿瘤抗原 PRAME 是黑色素瘤细胞中 p53 激活的潜在治疗靶点。

IF 2.9 3区生物学

BMB Reports Pub Date : 2024-06-01

Yong-Kyu Lee, Hyeon Ho Heo, Nackhyoung Kim, Ui-Hyun Park, Hyesook Youn, Eun-Yi Moon, Eun-Joo Kim, Soo-Jong Um

{"title":"Tumor antigen PRAME is a potential therapeutic target of p53 activation in melanoma cells.","authors":"Yong-Kyu Lee, Hyeon Ho Heo, Nackhyoung Kim, Ui-Hyun Park, Hyesook Youn, Eun-Yi Moon, Eun-Joo Kim, Soo-Jong Um","doi":"","DOIUrl":"","url":null,"abstract":"Upregulation of PRAME (preferentially expressed antigen of melanoma) has been implicated in the progression of a variety of cancers, including melanoma. The tumor suppressor p53 is a transcriptional regulator that mediates cell cycle arrest and apoptosis in response to stress signals. Here, we report that PRAME is a novel repressive target of p53. This was supported by analysis of melanoma cell lines carrying wild-type p53 and human melanoma databases. mRNA expression of PRAME was downregulated by p53 overexpression and activation using DNA-damaging agents, but upregulated by p53 depletion. We identified a p53-responsive element (p53RE) in the promoter region of PRAME. Luciferase and ChIP assays showed that p53 represses the transcriptional activity of the PRAME promoter and is recruited to the p53RE together with HDAC1 upon etoposide treatment. The functional significance of p53 activationmediated PRAME downregulation was demonstrated by measuring colony formation and p27 expression in melanoma cells. These data suggest that p53 activation, which leads to PRAME downregulation, could be a therapeutic strategy in melanoma cells. [BMB Reports 2024; 57(6): 299-304].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"299-304"},"PeriodicalIF":2.9,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11214892/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141247393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Genetic disruption of ATAT1 causes RhoA downregulation through abnormal truncation of C/EBPβ. ATAT1 的基因干扰会通过 C/EBPβ 的异常截断导致 RhoA 下调。

IF 2.9 3区生物学

BMB Reports Pub Date : 2024-06-01

Jee-Hye Choi, Jangho Jeong, Jaegu Kim, Eunae You, Seula Keum, Seongeun Song, Ye Eun Hwang, Minjoo Ji, Kwon-Sik Park, Sangmyung Rhee

{"title":"Genetic disruption of ATAT1 causes RhoA downregulation through abnormal truncation of C/EBPβ.","authors":"Jee-Hye Choi, Jangho Jeong, Jaegu Kim, Eunae You, Seula Keum, Seongeun Song, Ye Eun Hwang, Minjoo Ji, Kwon-Sik Park, Sangmyung Rhee","doi":"","DOIUrl":"","url":null,"abstract":"Microtubule acetylation has been shown to regulate actin filament dynamics by modulating signaling pathways that control actin organization, although the precise mechanisms remain unknown. In this study, we found that the downregulation of microtubule acetylation via the disruption ATAT1 (which encodes α-tubulin N-acetyltransferase 1) inhibited the expression of RhoA, a small GTPase involved in regulating the organization of actin filaments and the formation of stress fibers. Analysis of RHOA promoter and chromatin immunoprecipitation assays revealed that C/EBPβ is a major regulator of RHOA expression. Interestingly, the majority of C/EBPβ in ATAT1 knockout (KO) cells was found in the nucleus as a 27-kDa fragment (referred to as C/EBPβp27) lacking the N-terminus of C/EBPβ. Overexpression of a gene encoding a C/EBPβp27-mimicking protein via an N-terminal deletion in C/EBPβ led to competitive binding with wild-type C/EBPβ at the C/EBPβ binding site in the RHOA promoter, resulting in a significant decrease of RHOA expression. We also found that cathepsin L (CTSL), which is overexpressed in ATAT1 KO cells, is responsible for C/EBPβp27 formation in the nucleus. Treatment with a CTSL inhibitor led to the restoration of RHOA expression by downregulation of C/EBPβp27 and the invasive ability of ATAT1 KO MDA-MB-231 breast cancer cells. Collectively, our findings suggest that the downregulation of microtubule acetylation associated with ATAT1 deficiency suppresses RHOA expression by forming C/EBPβp27 in the nucleus through CTSL. We propose that CTSL and C/EBPβp27 may represent a novel therapeutic target for breast cancer treatment. [BMB Reports 2024; 57(6): 293-298].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"293-298"},"PeriodicalIF":2.9,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11214891/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141247381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Integrative analysis of microRNA-mediated mitochondrial dysfunction in hippocampal neural progenitor cell death in relation with Alzheimer's disease. 水凝胶药物疗法在黑色素瘤免疫疗法中的研究进展。

IF 2.9 3区生物学

BMB Reports Pub Date : 2024-06-01

A Reum Han, Tae Kwon Moon, Im Kyeung Kang, Dae Bong Yu, Yechan Kim, Cheolhwan Byon, Sujeong Park, Hae Lin Kim, Hae Lin Kim, Kyoung Jin Lee, Heuiran Lee, Ha-Na Woo, Seong Who Kim

{"title":"Integrative analysis of microRNA-mediated mitochondrial dysfunction in hippocampal neural progenitor cell death in relation with Alzheimer's disease.","authors":"A Reum Han, Tae Kwon Moon, Im Kyeung Kang, Dae Bong Yu, Yechan Kim, Cheolhwan Byon, Sujeong Park, Hae Lin Kim, Hae Lin Kim, Kyoung Jin Lee, Heuiran Lee, Ha-Na Woo, Seong Who Kim","doi":"","DOIUrl":"","url":null,"abstract":"Adult hippocampal neurogenesis plays a pivotal role in maintaining cognitive brain function. However, this process diminishes with age, particularly in patients with neurodegenerative disorders. While small, non-coding microRNAs (miRNAs) are crucial for hippocampal neural stem (HCN) cell maintenance, their involvement in neurodegenerative disorders remains unclear. This study aimed to elucidate the mechanisms through which miRNAs regulate HCN cell death and their potential involvement in neurodegenerative disorders. We performed a comprehensive microarray-based analysis to investigate changes in miRNA expression in insulin-deprived HCN cells as an in vitro model for cognitive impairment. miR-150-3p, miR-323-5p, and miR-370-3p, which increased significantly over time following insulin withdrawal, induced pronounced mitochondrial fission and dysfunction, ultimately leading to HCN cell death. These miRNAs collectively targeted the mitochondrial fusion protein OPA1, with miR-150-3p also targeting MFN2. Data-driven analyses of the hippocampi and brains of human subjects revealed significant reductions in OPA1 and MFN2 in patients with Alzheimer's disease (AD). Our results indicate that miR-150-3p, miR-323-5p, and miR-370-3p contribute to deficits in hippocampal neurogenesis by modulating mitochondrial dynamics. Our findings provide novel insight into the intricate connections between miRNA and mitochondrial dynamics, shedding light on their potential involvement in conditions characterized by deficits in hippocampal neurogenesis, such as AD. [BMB Reports 2024; 57(6): 281-286].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"281-286"},"PeriodicalIF":2.9,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11214893/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138486673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

CDKN2 expression is a potential biomarker for T cell exhaustion in hepatocellular carcinoma. CDKN2 表达是肝细胞癌中 T 细胞衰竭的潜在生物标志物。

IF 2.9 3区生物学

BMB Reports Pub Date : 2024-06-01

Shibo Wei, Yan Zhang, Baeki E Kang, Wonyoung Park, He Guo, Seungyoon Nam, Jong-Sun Kang, Jee-Heon Jeong, Yunju Jo, Dongryeol Ryu, Yikun Jiang, Ki-Tae Ha

{"title":"CDKN2 expression is a potential biomarker for T cell exhaustion in hepatocellular carcinoma.","authors":"Shibo Wei, Yan Zhang, Baeki E Kang, Wonyoung Park, He Guo, Seungyoon Nam, Jong-Sun Kang, Jee-Heon Jeong, Yunju Jo, Dongryeol Ryu, Yikun Jiang, Ki-Tae Ha","doi":"","DOIUrl":"","url":null,"abstract":"Hepatocellular Carcinoma (HCC), the predominant primary hepatic malignancy, is the prime contributor to mortality. Despite the availability of multiple surgical interventions, patient outcomes remain suboptimal. Immunotherapies have emerged as effective strategies for HCC treatment with multiple clinical advantages. However, their curative efficacy is not always satisfactory, limited by the dysfunctional T cell status. Thus, there is a pressing need to discover novel potential biomarkers indicative of T cell exhaustion (Tex) for personalized immunotherapies. One promising target is Cyclin-dependent kinase inhibitor 2 (CDKN2) gene, a key cell cycle regulator with aberrant expression in HCC. However, its specific involvement remains unclear. Herein, we assessed the potential of CDKN2 expression as a promising biomarker for HCC progression, particularly for exhausted T cells. Our transcriptome analysis of CDKN2 in HCC revealed its significant role involving in HCC development. Remarkably, single-cell transcriptomic analysis revealed a notable correlation between CDKN2 expression, particularly CDKN2A, and Tex markers, which was further validated by a human cohort study using human HCC tissue microarray, highlighting CDKN2 expression as a potential biomarker for Tex within the intricate landscape of HCC progression. These findings provide novel perspectives that hold promise for addressing the unmet therapeutic need within HCC treatment. [BMB Reports 2024; 57(6): 287-292].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"287-292"},"PeriodicalIF":2.9,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11214889/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140206329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Emerging paradigms in cancer cell plasticity. 癌细胞可塑性的新范例。

IF 2.9 3区生物学

BMB Reports Pub Date : 2024-06-01

Hyunbin D Huh, Hyun Woo Park

{"title":"Emerging paradigms in cancer cell plasticity.","authors":"Hyunbin D Huh, Hyun Woo Park","doi":"","DOIUrl":"","url":null,"abstract":"Cancer cells metastasize to distant organs by altering their characteristics within the tumor microenvironment (TME) to effectively overcome challenges during the multistep tumorigenesis. Plasticity endows cancer cell with the capacity to shift between different morphological states to invade, disseminate, and seed metastasis. The epithelial-to-mesenchymal transition (EMT) is a theory derived from tissue biopsy, which explains the acquisition of EMT transcription factors (TFs) that convey mesenchymal features during cancer migration and invasion. On the other hand, adherent-to-suspension transition (AST) is an emerging theory derived from liquid biopsy, which describes the acquisition of hematopoietic features by AST-TFs that reprograms anchorage dependency during the dissemination of circulating tumor cells (CTCs). The induction and plasticity of EMT and AST dynamically reprogram cell-cell interaction and cell-matrix interaction during cancer dissemination and colonization. Here, we review the mechanisms governing cellular plasticity of AST and EMT during the metastatic cascade and discuss therapeutic challenges posed by these two morphological adaptations to provide insights for establishing new therapeutic interventions. [BMB Reports 2024; 57(6): 273-280].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"273-280"},"PeriodicalIF":2.9,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11214895/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140874453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

3D epigenomics and 3D epigenopathies. 三维表观基因组学和三维表观基因病。

IF 2.9 3区生物学

BMB Reports Pub Date : 2024-05-01

Kyung-Hwan Lee, Jungyu Kim, Ji Hun Kim

引用次数: 0

Cisd2 deficiency impairs neutrophil function by regulating calcium homeostasis via Calnexin and SERCA. Cisd2 缺乏症通过 Calnexin 和 SERCA 调节钙稳态，从而损害中性粒细胞的功能。

IF 2.9 3区生物学

BMB Reports Pub Date : 2024-05-01

Un Yung Choi, Youn Jung Choi, Shin-Ae Lee, Ji-Seung Yoo

{"title":"Cisd2 deficiency impairs neutrophil function by regulating calcium homeostasis via Calnexin and SERCA.","authors":"Un Yung Choi, Youn Jung Choi, Shin-Ae Lee, Ji-Seung Yoo","doi":"","DOIUrl":"","url":null,"abstract":"In the context of aging, the susceptibility to infectious diseases increases, leading to heightened morbidity and mortality. This phenomenon, termed immunosenescence, is characterized by dysregulation in the aging immune system, including abnormal alterations in lymphocyte composition, elevated basal inflammation, and the accumulation of senescent T cells. Such changes contribute to increased autoimmune diseases, enhanced infection severity, and reduced responsiveness to vaccines. Utilizing aging animal models becomes imperative for a comprehensive understanding of immunosenescence, given the complexity of aging as a physiological process in living organisms. Our investigation focuses on Cisd2, a causative gene for Wolfram syndrome, to elucidate on immunosenescence. Cisd2 knockout (KO) mice, serving as a model for premature aging, exhibit a shortened lifespan with early onset of aging-related features, such as decreased bone density, hair loss, depigmentation, and optic nerve degeneration. Intriguingly, we found that the Cisd2 KO mice present a higher number of neutrophils in the blood; however, isolated neutrophils from these mice display functional defects. Through mass spectrometry analysis, we identified an interaction between Cisd2 and Calnexin, a protein known for its role in protein quality control. Beyond this function, Calnexin also regulates calcium homeostasis through interaction with sarcoendoplasmic reticulum calcium transport ATPase (SERCA). Our study proposes that Cisd2 modulates calcium homeostasis via its interaction with Calnexin and SERCA, consequently influencing neutrophil functions. [BMB Reports 2024; 57(5): 256-261].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"256-261"},"PeriodicalIF":2.9,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11139677/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140847976","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

BAP1 controls mesenchymal stem cell migration by inhibiting the ERK signaling pathway. BAP1通过抑制ERK信号通路控制间充质干细胞迁移。

IF 2.9 3区生物学

BMB Reports Pub Date : 2024-05-01

Seobin Kim, Eun-Woo Lee, Doo-Byoung Oh, Jinho Seo

{"title":"BAP1 controls mesenchymal stem cell migration by inhibiting the ERK signaling pathway.","authors":"Seobin Kim, Eun-Woo Lee, Doo-Byoung Oh, Jinho Seo","doi":"","DOIUrl":"","url":null,"abstract":"Due to their stem-like characteristics and immunosuppressive properties, Mesenchymal stem cells (MSCs) offer remarkable potential in regenerative medicine. Much effort has been devoted to enhancing the efficacy of MSC therapy by enhancing MSC migration. In this study, we identified deubiquitinase BRCA1- associated protein 1 (BAP1) as an inhibitor of MSC migration. Using deubiquitinase siRNA library screening based on an in vitro wound healing assay, we found that silencing BAP1 significantly augmented MSC migration. Conversely, BAP1 overexpression reduced the migration and invasion capabilities of MSCs. BAP1 depletion in MSCs upregulates ERK phosphorylation, thereby increasing the expression of the migration factor, osteopontin. Further examination revealed that BAP1 interacts with phosphorylated ERK1/2, deubiquitinating their ubiquitins, and thus attenuating the ERK signaling pathway. Overall, our study highlights the critical role of BAP1 in regulating MSC migration through its deubiquitinase activity, and suggests a novel approach to improve the therapeutic potential of MSCs in regenerative medicine. [BMB Reports 2024; 57(5): 250-255].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"250-255"},"PeriodicalIF":2.9,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11139679/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"107590063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Single-cell RNA sequencing reveals the heterogeneity of adipose tissue-derived mesenchymal stem cells under chondrogenic induction. 单细胞RNA测序揭示了软骨诱导下脂肪组织来源的间充质干细胞的异质性。

IF 2.9 3区生物学

BMB Reports Pub Date : 2024-05-01

Jeewan Chun, Ji-Hoi Moon, Kyu Hwan Kwack, Eun-Young Jang, Saebyeol Lee, Hak Kyun Kim, Jae-Hyung Lee

{"title":"Single-cell RNA sequencing reveals the heterogeneity of adipose tissue-derived mesenchymal stem cells under chondrogenic induction.","authors":"Jeewan Chun, Ji-Hoi Moon, Kyu Hwan Kwack, Eun-Young Jang, Saebyeol Lee, Hak Kyun Kim, Jae-Hyung Lee","doi":"","DOIUrl":"","url":null,"abstract":"This study investigated how adipose tissue-derived mesenchymal stem cells (AT-MSCs) respond to chondrogenic induction using droplet-based single-cell RNA sequencing (scRNA-seq). We analyzed 37,219 high-quality transcripts from control cells and cells induced for 1 week (1W) and 2 weeks (2W). Four distinct cell clusters (0-3), undetectable by bulk analysis, exhibited varying proportions. Cluster 1 dominated in control and 1W cells, whereas clusters (3, 2, and 0) exclusively dominated in control, 1W, and 2W cells, respectively. Furthermore, heterogeneous chondrogenic markers expression within clusters emerged. Gene ontology (GO) enrichment analysis of differentially expressed genes unveiled cluster-specific variations in key biological processes (BP): (1) Cluster 1 exhibited up-regulation of GO-BP terms related to ribosome biogenesis and translational control, crucial for maintaining stem cell properties and homeostasis; (2) Additionally, cluster 1 showed up-regulation of GO-BP terms associated with mitochondrial oxidative metabolism; (3) Cluster 3 displayed up-regulation of GO-BP terms related to cell proliferation; (4) Clusters 0 and 2 demonstrated similar up-regulation of GO-BP terms linked to collagen fibril organization and supramolecular fiber organization. However, only cluster 0 showed a significant decrease in GO-BP terms related to ribosome production, implying a potential correlation between ribosome regulation and the differentiation stages of AT-MSCs. Overall, our findings highlight heterogeneous cell clusters with varying balances between proliferation and differentiation before, and after, chondrogenic stimulation. This provides enhanced insights into the single-cell dynamics of AT-MSCs during chondrogenic differentiation. [BMB Reports 2024; 57(5): 232-237].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"232-237"},"PeriodicalIF":2.9,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11139680/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71420408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0