IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-06-05 DOI: 10.1080/15384101.2025.2514988

Shanshan Jia, Nian Shi, Meiqi Lu, Xiaoyang Wang, Yongjun Qi, Xiaochuan Wang, Jie Zhao, Duyin Jiang

引用次数: 0

Hair-follicle-associated pluripotent (HAP) stem-cell-sheet implantation accelerates cutaneous wound closure and suppresses scar formation in a mouse model. 在小鼠模型中，毛囊相关多能干细胞片植入加速皮肤伤口愈合并抑制疤痕形成。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-05-27 DOI: 10.1080/15384101.2025.2508112

Koya Obara, Kyoko Baba, Kyoumi Shirai, Yuko Hamada, Nobuko Arakawa, Ayami Hasegawa, Nanako Takaoka, Ryoichi Aki, Robert M Hoffman

{"title":"Hair-follicle-associated pluripotent (HAP) stem-cell-sheet implantation accelerates cutaneous wound closure and suppresses scar formation in a mouse model.","authors":"Koya Obara, Kyoko Baba, Kyoumi Shirai, Yuko Hamada, Nobuko Arakawa, Ayami Hasegawa, Nanako Takaoka, Ryoichi Aki, Robert M Hoffman","doi":"10.1080/15384101.2025.2508112","DOIUrl":"https://doi.org/10.1080/15384101.2025.2508112","url":null,"abstract":"Patients frequently experience physical, mental, and even financial distress because of acute or chronic skin wounds. In severe situations, scarring on the skin can be quite noticeable, cause persistent discomfort, restrict joint motion, or be mentally taxing. Hair-follicle-associated pluripotent (HAP) stem cells were discovered by our laboratory, in the bulge area of the hair follicle and can differentiate to neurons, glia, beating cardiomyocytes, keratinocytes and nascent vessels. In the present study, HAP stem cell sheets were formed by culturing the upper part of hair follicles and implanting into mice with skin ulcers. The HAP stem cell sheets contained keratinocytes, endothelial cells and neurons. Autologous HAP stem cell sheet implantation to the dorsal wound in C57BL/6J mice significantly accelerated wound closure compared with non-implanted control mice. HAP-stem-cell sheets expressing green fluorescent protein (GFP) implanted into nude mice differentiated into keratinocytes in the epidermis, and neurons and endothelial cells in the dermis. The thicknesses of the epidermis and dermis and M2 macrophage and myofibroblast infiltration into the wound were significantly decreased in HAP-stem cell-implanted mice compared with non-implanted control mice. Expression levels of TGF-β1, COL1A2 and COL3A1 mRNA in the wound were significantly decreased in HAP stem cell-implanted mice compared with non-implanted control mice. These results suggest that implanting HAP stem cell sheets accelerates cutaneous wound closure and suppresses scar formation. The HAP stem cells used in the present study thus have potential as a future clinical strategy for accelerating wound healing.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-14"},"PeriodicalIF":3.4,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155883","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}

引用次数: 0

Cell-cycle dependent inhibition of BRCA1 signaling by the lysine methyltransferase SET8. 赖氨酸甲基转移酶SET8对BRCA1信号的细胞周期依赖性抑制。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-05-22 DOI: 10.1080/15384101.2025.2508114

Yannick Perez, Fatima Alhourani, Julie Patouillard, Cyril Ribeyre, Marion Larroque, Véronique Baldin, David Lleres, Charlotte Grimaud, Eric Julien

{"title":"Cell-cycle dependent inhibition of BRCA1 signaling by the lysine methyltransferase SET8.","authors":"Yannick Perez, Fatima Alhourani, Julie Patouillard, Cyril Ribeyre, Marion Larroque, Véronique Baldin, David Lleres, Charlotte Grimaud, Eric Julien","doi":"10.1080/15384101.2025.2508114","DOIUrl":"10.1080/15384101.2025.2508114","url":null,"abstract":"The cell-cycle regulated methyltransferase SET8 is the sole enzyme responsible for the mono-methylation of histone H4 at lysine 20 (H4K20) that is the substrate for di- and trimethylation mainly by SUV4-20Hs enzymes. Both SET8 and SUV4-20Hs have been implicated in regulating DNA repair pathway choice through the inverse affinities of BRCA1-BARD1 and 53BP1 complexes for disparate methylation states of H4K20. However, the precise and respective functions of each H4K20 methyltransferase in DNA repair pathways remain to be clarified. Here, we show that SET8 acts as a potent chromatin inhibitor of homologous recombination and that its timely degradation during DNA replication is essential for the spontaneous nuclear focal accumulation of BRCA1 and RAD51 complexes during the S phase. Strikingly, the anti-recombinogenic function of SET8 is independent of SUV4-20H activity but requires the subsequent recruitment of the ubiquitin ligase RNF168. Moreover, we show that SET8-induced BRCA1 inhibition is not necessarily related to the loss of BARD1 binding to unmethylated histone H4K20. Instead, it is largely caused by the accumulation of 53BP1 in a manner depending on the concerted activities of SET8 and RNF168 on chromatin. Conversely, the lack of SET8 and H4K20 mono-methylation on newly assembly chromatin after DNA replication led to the untimely accumulation of BRCA1 on chromatin at the subsequent G1 phase. Altogether, these results establish the de novo activity of SET8 on chromatin as a primordial epigenetic lock of the BRCA1-mediated HR pathway during the cell cycle.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-23"},"PeriodicalIF":3.4,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144126933","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}

引用次数: 0

Succinate reduces biological activity and mitochondrial function of human adipose-derived stem cells. 琥珀酸盐降低人脂肪干细胞的生物活性和线粒体功能。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-05-20 DOI: 10.1080/15384101.2025.2508109

Bo Wang, Xinxin Wang, Meijin Guo, Huiming Xu

{"title":"Succinate reduces biological activity and mitochondrial function of human adipose-derived stem cells.","authors":"Bo Wang, Xinxin Wang, Meijin Guo, Huiming Xu","doi":"10.1080/15384101.2025.2508109","DOIUrl":"https://doi.org/10.1080/15384101.2025.2508109","url":null,"abstract":"Elevated succinate accumulation has been demonstrated to be associated with metabolic and inflammatory disorders. Our previous study revealed that adipose-derived stem cells (ADSC) from obese individuals exhibit high succinate, reduced biological activity, and mitochondrial dysfunction. However, the precise role of succinate in these processes remains unclear. Here, we investigated the effects of excess succinate on cellular biological activity, immunomodulatory capacity, and mitochondrial function of ADSC. We found that elevated succinate levels in ADSC decreased proliferation and differentiation potential, while promoting M1 macrophage polarization. Furthermore, succinate accumulation impaired mitochondrial biogenesis and metabolism, increasing in reactive oxygen species (ROS) production and inflammatory responses. Transcriptome sequencing analysis further confirmed that succinate upregulated inflammatory pathways, suppressed mitochondrial biogenesis and metabolism, and enhanced cellular apoptosis and senescence, accompanied by reduced DNA replication and repair. Overall, these findings imply that succinate accumulation in ADSC triggers inflammatory response and mitochondrial dysfunction, potentially contributing to a decline of cellular biological activity. Targeting succinate may offer therapeutic potential for metabolic disorders.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-13"},"PeriodicalIF":3.4,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144109873","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}

引用次数: 0

Statement of Retraction: Human umbilical cord mesenchymal stem cell-derived exosome-mediated transfer of microRNA-133b boosts trophoblast cell proliferation, migration and invasion in preeclampsia by restricting SGK1. 撤回声明：人脐带间充质干细胞衍生的外泌体介导的microRNA-133b转移通过限制SGK1促进滋养细胞增殖、迁移和侵袭子痫前期。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-05-19 DOI: 10.1080/15384101.2025.2506290

引用次数: 0

Statement of Retraction: LncRNA XIST promotes human lung adenocarcinoma cells to cisplatin resistance via let-7i/BAG-1 axis. 撤回声明：LncRNA XIST通过let-7i/BAG-1轴促进人肺腺癌细胞产生顺铂耐药。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-04-29 DOI: 10.1080/15384101.2025.2460938

引用次数: 0

Regulation of microtubule growth rates and their impact on chromosomal instability. 微管生长速率的调控及其对染色体不稳定性的影响。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-04-22 DOI: 10.1080/15384101.2025.2485842

Lia Mara Gomes Paim, Susanne Bechstedt

{"title":"Regulation of microtubule growth rates and their impact on chromosomal instability.","authors":"Lia Mara Gomes Paim, Susanne Bechstedt","doi":"10.1080/15384101.2025.2485842","DOIUrl":"https://doi.org/10.1080/15384101.2025.2485842","url":null,"abstract":"Microtubules are polymers of α/β tubulin dimers that build the mitotic spindle, which segregates duplicated chromosomes during cell division. Microtubule function is governed by dynamic instability, whereby cycles of growth and shrinkage contribute to the forces necessary for chromosome movement. Regulation of microtubule growth velocity requires cell cycle-dependent changes in expression, localization and activity of microtubule-associated proteins (MAPs) as well as tubulin post-translational modifications that modulate microtubule dynamics. It has become clear that optimal microtubule growth velocities are required for proper chromosome segregation and ploidy maintenance. Suboptimal microtubule growth rates can result from altered activity of MAPs and could lead to aneuploidy, possibly by disrupting the establishment of microtubule bundles at kinetochores and altering the mechanical forces required for sister chromatid segregation. Future work using high-resolution, low-phototoxicity microscopy and novel fluorescent markers will be invaluable in obtaining deeper mechanistic insights into how microtubule processes contribute to chromosome segregation.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-20"},"PeriodicalIF":3.4,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143965776","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}

引用次数: 0

The SGLT2 inhibitor canagliflozin attenuates mitochondrial oxidative stress and alterations of calcium handling induced by high glucose in human cardiac fibroblasts. SGLT2抑制剂canagliflozin可减轻人心脏成纤维细胞高糖诱导的线粒体氧化应激和钙处理的改变。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-04-21 DOI: 10.1080/15384101.2025.2492423

Fahimeh Varzideh, Urna Kansakar, Scott Wilson, Stanislovas S Jankauskas, Gaetano Santulli

{"title":"The SGLT2 inhibitor canagliflozin attenuates mitochondrial oxidative stress and alterations of calcium handling induced by high glucose in human cardiac fibroblasts.","authors":"Fahimeh Varzideh, Urna Kansakar, Scott Wilson, Stanislovas S Jankauskas, Gaetano Santulli","doi":"10.1080/15384101.2025.2492423","DOIUrl":"https://doi.org/10.1080/15384101.2025.2492423","url":null,"abstract":"Cardiac fibrosis and remodeling are critical contributors to heart failure, particularly in the context of diabetes, where hyperglycemia (HG) exacerbates pathological fibroblast activity. Despite the known cardiovascular benefits of canagliflozin (CANA), its specific effects on human cardiac fibroblasts (HCFs) under HG conditions remain unexplored. We investigated whether CANA could mitigate HG-induced detrimental responses in HCFs. Dose-response assays revealed that 100 nM CANA significantly reduced HG-induced proliferation and migration of HCFs. Furthermore, CANA attenuated mitochondrial reactive oxygen species (ROS) production, a key driver of myofibroblast differentiation, and suppressed HG-induced expression of SMAD2, a critical activator of cardiac fibroblasts. Additionally, HG disrupted calcium (Ca2+) homeostasis, which was ameliorated by CANA treatment. These findings collectively demonstrate that CANA exerts protective effects on HCFs by improving mitochondrial function, restoring Ca2+ handling, and reducing fibroblast proliferation, migration, and activation under HG conditions.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-8"},"PeriodicalIF":3.4,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143986404","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}

引用次数: 0

The involvement of cyclin-dependent kinase 7 (CDK7) and 9 (CDK9) in coordinating transcription and cell cycle checkpoint regulation. 细胞周期蛋白依赖性激酶7 （CDK7）和9 （CDK9）参与协调转录和细胞周期检查点调节。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-04-14 DOI: 10.1080/15384101.2025.2485844

Cheng-Fan Lee, Kenneth J Pienta, Sarah R Amend

{"title":"The involvement of cyclin-dependent kinase 7 (CDK7) and 9 (CDK9) in coordinating transcription and cell cycle checkpoint regulation.","authors":"Cheng-Fan Lee, Kenneth J Pienta, Sarah R Amend","doi":"10.1080/15384101.2025.2485844","DOIUrl":"https://doi.org/10.1080/15384101.2025.2485844","url":null,"abstract":"Cells regulate the expression of cell cycle-related genes, including cyclins essential for mitosis, through the transcriptional activity of the positive transcription elongation factor b (P-TEFb), a complex comprising CDK9, cyclin T, and transcription factors. P-TEFb cooperates with CDK7 to activate RNA polymerase. In response to DNA stress, the cell cycle shifts from mitosis to repair, triggering cell cycle arrest and the activation of DNA repair genes. This tight coordination between transcription, cell cycle progression, and DNA stress response is crucial for maintaining cellular integrity. Cyclin-dependent kinases CDK7 and CDK9 are central to both transcription and cell cycle regulation. CDK7 functions as the CDK-activating kinase (CAK), essential for activating other CDKs, while CDK9 acts as a critical integrator of signals from both the cell cycle and transcriptional machinery. This review elucidates the mechanisms by which CDK7 and CDK9 regulate the mitotic process and cell cycle checkpoints, emphasizing their roles in balancing cell growth, homeostasis, and DNA repair through transcriptional control.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-13"},"PeriodicalIF":3.4,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143981567","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}

引用次数: 0

α-Fodrin-CENP-E interaction is critical for pancreatic cancer progression and drug response. α-Fodrin-CENP-E相互作用对胰腺癌进展和药物反应至关重要。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-04-10 DOI: 10.1080/15384101.2025.2485837

Athira Jyothy, Julfequar Hussain, Sharanya C S, Vineetha Radhakrishnan Chandraprabha, Madhumathy G Nair, Smreti Vasudevan, Hariharan Sreedharan, Betty Abraham, Tessy Thomas Maliekal, Kathiresan Natarajan, Suparna Sengupta

{"title":"α-Fodrin-CENP-E interaction is critical for pancreatic cancer progression and drug response.","authors":"Athira Jyothy, Julfequar Hussain, Sharanya C S, Vineetha Radhakrishnan Chandraprabha, Madhumathy G Nair, Smreti Vasudevan, Hariharan Sreedharan, Betty Abraham, Tessy Thomas Maliekal, Kathiresan Natarajan, Suparna Sengupta","doi":"10.1080/15384101.2025.2485837","DOIUrl":"https://doi.org/10.1080/15384101.2025.2485837","url":null,"abstract":"α-Fodrin, a known scaffolding protein for cytoskeleton stabilization, performs various functions including cell adhesion, cell motility, DNA repair and apoptosis. Based on our previous results revealing its role in mitosis in glioblastoma, we have examined its effect in pancreatic cancer, which is often linked to mitotic aberrations including aneuploidy and chromosome instability. Here, we show that the expression of α-Fodrin increases in pancreatic adenocarcinoma tissues compared to its normal counterpart, suggesting its tumor promoting role. shRNA-mediated knock-down of α-Fodrin significantly reduces the xenograft growth in immunocompromised mice underscoring the importance of α-Fodrin in tumor progression. CENP-E (centromere-associated protein E) is a motor protein essential for chromosomal alignment and segregation during mitosis. We have found that α-Fodrin interacts with CENP-E to recruit it to the kinetochore and depletion of α-Fodrin has a crucial role in controlling aneuploidy. As these mitotic defects can lead to apoptosis, we have further evaluated the activation of possible upstream pathways. Paclitaxel, a chemotherapeutic agent that stabilizes microtubules, disrupts mitosis and induces apoptosis. We found that Paclitaxel triggered stronger activation of JNK, ERK, and P38 MAPKs, altered BCL2/BAX ratios, cytochrome C release causing increased apoptosis in α-Fodrin knockdown cells compared to cells with wild-type α-Fodrin. This enhanced sensitivity to paclitaxel is consistent with improved survival in pancreatic cancer patients with low α-Fodrin (SPTAN1) and low CENP-E expression compared to poor prognosis with high expressions of both the genes. Taken together, this study provides the molecular mechanism by which α-Fodrin - CENP-E axis regulates pancreatic cancer progression and drug response.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-25"},"PeriodicalIF":3.4,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143954791","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}

引用次数: 0

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