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Contemporaneous Inflammatory, Angiogenic, Fibrogenic, and Angiostatic Cytokine Profiles of the Time-to-Tumor Development by Cancer Cells to Orchestrate Tumor Neovascularization, Progression, and Metastasis. 癌细胞在肿瘤发展过程中同时出现的炎症、血管生成、纤维生成和血管静止细胞因子谱,可协调肿瘤血管新生、进展和转移。
IF 5.1 2区 生物学
Cells Pub Date : 2024-10-20 DOI: 10.3390/cells13201739
Elizabeth Skapinker, Emilyn B Aucoin, Haley L Kombargi, Abdulrahman M Yaish, Yunfan Li, Leili Baghaie, Myron R Szewczuk
{"title":"Contemporaneous Inflammatory, Angiogenic, Fibrogenic, and Angiostatic Cytokine Profiles of the Time-to-Tumor Development by Cancer Cells to Orchestrate Tumor Neovascularization, Progression, and Metastasis.","authors":"Elizabeth Skapinker, Emilyn B Aucoin, Haley L Kombargi, Abdulrahman M Yaish, Yunfan Li, Leili Baghaie, Myron R Szewczuk","doi":"10.3390/cells13201739","DOIUrl":"https://doi.org/10.3390/cells13201739","url":null,"abstract":"<p><p>Cytokines can promote various cancer processes, such as angiogenesis, epithelial to mesenchymal transition (EMT), invasion, and tumor progression, and maintain cancer stem-cell-like (CSCs) cells. The mechanism(s) that continuously promote(s) tumors to progress in the TME still need(s) to be investigated. The data in the present study analyzed the inflammatory, angiogenic, fibrogenic, and angiostatic cytokine profiles in the host serum during tumor development in a mouse model of human pancreatic cancer. Pancreatic MiaPaCa-2-eGFP cancer cells were subcutaneously implanted in RAG2xCγ double mutant mice. Blood samples were collected before cancer cell implantation and every week until the end point of the study. The extracted serum from the blood of each mouse at different time points during tumor development was analyzed using a Bio-Plex microarray analysis and a Bio-Plex 200 system for proinflammatory (IL-1β, IL-10, IFN-γ, and TNF-α) and angiogenic and fibrogenic (IL-15, IL-18, basic FGF, LIF, M-CSF, MIG, MIP-2, PDGF-BB, and VEGF) cytokines. Here, we find that during cancer cell colonization for tumor development, host angiogenic, fibrogenic, and proinflammatory cytokine profiling in the tumor-bearing mice has been shown to significantly reduce host angiostatic and proinflammatory cytokines that restrain tumor development and increase those for tumor growth. The proinflammatory cytokines IL-15, IL-18, and IL-1β profiles reveal a significant host serum increase after day 35 when the tumor began to progress in growth. In contrast, the angiostatic cytokine profiles of TNFα, MIG, M-CSF, IL-10, and IFNγ in the host serum revealed a dramatic and significant decrease after day 5 post-implantation of cancer cells. OP treatment of tumor-bearing mice on day 35 maintained high levels of angiostatic and fibrogenic cytokines. The data suggest an entirely new regulation by cancer cells for tumor development. The findings identify for the first time how pancreatic cancer cells use host cytokine profiling to orchestrate the initiation of tumor development.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"13 20","pages":""},"PeriodicalIF":5.1,"publicationDate":"2024-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11506673/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495935","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}
引用次数: 0
Apolipoprotein-L1 (APOL1): From Sleeping Sickness to Kidney Disease. 载脂蛋白-L1 (APOL1):从睡病到肾病。
IF 5.1 2区 生物学
Cells Pub Date : 2024-10-20 DOI: 10.3390/cells13201738
Etienne Pays
{"title":"Apolipoprotein-L1 (APOL1): From Sleeping Sickness to Kidney Disease.","authors":"Etienne Pays","doi":"10.3390/cells13201738","DOIUrl":"https://doi.org/10.3390/cells13201738","url":null,"abstract":"<p><p>Apolipoprotein-L1 (APOL1) is a membrane-interacting protein induced by inflammation, which confers human resistance to infection by African trypanosomes. APOL1 kills <i>Trypanosoma brucei</i> through induction of apoptotic-like parasite death, but two <i>T. brucei</i> clones acquired resistance to APOL1, allowing them to cause sleeping sickness. An APOL1 C-terminal sequence alteration, such as occurs in natural West African variants G1 and G2, restored human resistance to these clones. However, APOL1 unfolding induced by G1 or G2 mutations enhances protein hydrophobicity, resulting in kidney podocyte dysfunctions affecting renal filtration. The mechanism involved in these dysfunctions is debated. The ability of APOL1 to generate ion pores in trypanosome intracellular membranes or in synthetic membranes was provided as an explanation. However, transmembrane insertion of APOL1 strictly depends on acidic conditions, and podocyte cytopathology mainly results from secreted APOL1 activity on the plasma membrane, which occurs under non-acidic conditions. In this review, I argue that besides inactivation of APOL3 functions in membrane dynamics (fission and fusion), APOL1 variants induce inflammation-linked podocyte toxicity not through pore formation, but through plasma membrane disturbance resulting from increased interaction with cholesterol, which enhances cation channels activity. A natural mutation in the membrane-interacting domain (N264K) abrogates variant APOL1 toxicity at the expense of slightly increased sensitivity to trypanosomes, further illustrating the continuous mutual adaptation between host and parasite.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"13 20","pages":""},"PeriodicalIF":5.1,"publicationDate":"2024-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11506758/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495910","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}
引用次数: 0
The Utilization of PRAME in the Diagnosis, Prognosis, and Treatment of Melanoma. 在黑色素瘤的诊断、预后和治疗中使用 PRAME。
IF 5.1 2区 生物学
Cells Pub Date : 2024-10-20 DOI: 10.3390/cells13201740
Samuel L Blount, Xiaochen Liu, Jeffrey D McBride
{"title":"The Utilization of PRAME in the Diagnosis, Prognosis, and Treatment of Melanoma.","authors":"Samuel L Blount, Xiaochen Liu, Jeffrey D McBride","doi":"10.3390/cells13201740","DOIUrl":"https://doi.org/10.3390/cells13201740","url":null,"abstract":"<p><p>Melanoma, a deadly form of skin cancer, has seen improved survival rates due to advances in diagnosis and treatment, yet the need for further improvement remains critical. Tumor-associated antigens, such as PRAME (Preferentially Expressed Antigen in Melanoma), offer promising avenues for enhanced diagnostic precision, prognostic assessment, and targeted immunotherapy. PRAME, a cancer testis antigen, is selectively expressed in various cancers, including melanoma, and plays a key role in promoting tumorigenesis through inhibition of retinoic acid signaling, epithelial-to-mesenchymal transition, and immune evasion. This review explores the diagnostic utility of PRAME in distinguishing melanoma from benign nevi, its prognostic value in aggressive melanoma subtypes, and its potential as a therapeutic target in cancer vaccines and adoptive T-cell therapies. While PRAME-targeted therapies face challenges such as tumor heterogeneity and immune suppression, ongoing research aims to overcome these barriers, offering hope for more effective melanoma treatments.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"13 20","pages":""},"PeriodicalIF":5.1,"publicationDate":"2024-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11505691/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495969","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}
引用次数: 0
L-PGDS-PGD2-DP1 Axis Regulates Phagocytosis by CD36+ MGs/MΦs That Are Exclusively Present Within Ischemic Areas After Stroke. L-PGDS-PGD2-DP1轴调控仅存在于脑卒中后缺血区的CD36+ MGs/MΦ的吞噬作用
IF 5.1 2区 生物学
Cells Pub Date : 2024-10-20 DOI: 10.3390/cells13201737
Takayuki Nakagomi, Aya Narita, Hideaki Nishie, Akiko Nakano-Doi, Toshinori Sawano, Yu Fukuda, Tomohiro Matsuyama
{"title":"L-PGDS-PGD2-DP1 Axis Regulates Phagocytosis by CD36<sup>+</sup> MGs/MΦs That Are Exclusively Present Within Ischemic Areas After Stroke.","authors":"Takayuki Nakagomi, Aya Narita, Hideaki Nishie, Akiko Nakano-Doi, Toshinori Sawano, Yu Fukuda, Tomohiro Matsuyama","doi":"10.3390/cells13201737","DOIUrl":"https://doi.org/10.3390/cells13201737","url":null,"abstract":"<p><p>Brain injuries, such as ischemic stroke, cause cell death. Although phagocytosis of cellular debris is mainly performed by microglia/macrophages (MGs/MΦs), excessive accumulation beyond their phagocytic capacities results in waste product buildup, delaying brain cell regeneration. Therefore, it is essential to increase the potential for waste product removal from damaged brains. Lipocalin-type prostaglandin D synthase (L-PGDS) is the primary synthase for prostaglandin D2 (PGD2) and has been reported as a scavenger of waste products. However, the mechanism by which the L-PGDS-PGD2 axis exerts such an effect remains unelucidated. In this study, using a mouse model of ischemic stroke, we found that L-PGDS and its downstream signaling pathway components, including PGD2 and PGD2 receptor DP1 (but not DP2), were significantly upregulated in ischemic areas. Immunohistochemistry revealed the predominant expression of L-PGDS in the leptomeninges of ischemic areas and high expression levels of DP1 in CD36<sup>+</sup> MGs/MΦs that were specifically present within ischemic areas. Furthermore, PGD2 treatment promoted the conversion of MGs/MΦs into CD36<sup>+</sup> scavenger types and increased phagocytic activities of CD36<sup>+</sup> MGs/MΦs. Because CD36<sup>+</sup> MGs/MΦs specifically appeared within ischemic areas after stroke, our findings suggest that the L-PGDS-PGD2-DP1 axis plays an important role in brain tissue repair by regulating phagocytic activities of CD36<sup>+</sup> MGs/MΦs.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"13 20","pages":""},"PeriodicalIF":5.1,"publicationDate":"2024-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11505914/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495919","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}
引用次数: 0
Excess Potassium Promotes Autophagy to Maintain the Immunosuppressive Capacity of Myeloid-Derived Suppressor Cells Independent of Arginase 1. 过量的钾促进自噬以维持髓系衍生抑制细胞的免疫抑制能力,而不依赖于精氨酸酶 1。
IF 5.1 2区 生物学
Cells Pub Date : 2024-10-19 DOI: 10.3390/cells13201736
Ramesh Thylur Puttalingaiah, Matthew J Dean, Liqin Zheng, Phaethon Philbrook, Dorota Wyczechowska, Timothy Kayes, Luis Del Valle, Denise Danos, Maria Dulfary Sanchez-Pino
{"title":"Excess Potassium Promotes Autophagy to Maintain the Immunosuppressive Capacity of Myeloid-Derived Suppressor Cells Independent of Arginase 1.","authors":"Ramesh Thylur Puttalingaiah, Matthew J Dean, Liqin Zheng, Phaethon Philbrook, Dorota Wyczechowska, Timothy Kayes, Luis Del Valle, Denise Danos, Maria Dulfary Sanchez-Pino","doi":"10.3390/cells13201736","DOIUrl":"https://doi.org/10.3390/cells13201736","url":null,"abstract":"<p><p>Potassium ions (K<sup>+</sup>) are critical electrolytes that regulate multiple functions in immune cells. Recent studies have shown that the elevated concentration of extracellular potassium in the tumor interstitial fluid limits T cell effector function and suppresses the anti-tumor capacity of tumor-associated macrophages (TAMs). The effect of excess potassium on the biology of myeloid-derived suppressor cells (MDSCs), another important immune cell component of the tumor microenvironment (TME), is unknown. Here, we present data showing that increased concentrations of potassium chloride (KCl), as the source of K<sup>+</sup> ions, facilitate autophagy by increasing the expression of the autophagosome marker LC3β. Simultaneously, excess potassium ions significantly decrease the expression of arginase I (Arg I) and inducible nitric oxide synthase (iNOS) without reducing the ability of MDSCs to suppress T cell proliferation. Further investigation reveals that excess K<sup>+</sup> ions decrease the expression of the transcription factor C/EBP-β and alter the expression of phosphorylated kinases. While excess K<sup>+</sup> ions downregulated the expression levels of phospho-AMPKα (pAMPKα), it increased the levels of pAKT and pERK. Additionally, potassium increased mitochondrial respiration as measured by the oxygen consumption rate (OCR). Interestingly, all these alterations induced by K<sup>+</sup> ions were abolished by the autophagy inhibitor 3-methyladenine (3-MA). Our results suggest that hyperosmotic stress caused by excess K<sup>+</sup> ions regulate the mitochondrial respiration and signaling pathways in MDSCs to trigger the process of autophagy to support MDSCs' immunosuppressive function by mechanisms independent of Arg I and iNOS. Overall, our in vitro and ex vivo findings offer valuable insights into the adaptations of MDSCs within the K<sup>+</sup> ion-rich TME, which has important implications for MDSCs-targeted therapies.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"13 20","pages":""},"PeriodicalIF":5.1,"publicationDate":"2024-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11505641/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495957","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}
引用次数: 0
AREG Upregulation in Cancer Cells via Direct Interaction with Cancer-Associated Fibroblasts Promotes Esophageal Squamous Cell Carcinoma Progression Through EGFR-Erk/p38 MAPK Signaling. 通过与癌症相关成纤维细胞的直接相互作用,AREG 在癌细胞中上调,并通过表皮生长因子受体-Erk/p38 MAPK 信号转导促进食管鳞状细胞癌的进展。
IF 5.1 2区 生物学
Cells Pub Date : 2024-10-19 DOI: 10.3390/cells13201733
Takashi Nakanishi, Yu-Ichiro Koma, Shoji Miyako, Rikuya Torigoe, Hiroki Yokoo, Masaki Omori, Keitaro Yamanaka, Nobuaki Ishihara, Shuichi Tsukamoto, Takayuki Kodama, Mari Nishio, Manabu Shigeoka, Hiroshi Yokozaki, Yoshihiro Kakeji
{"title":"AREG Upregulation in Cancer Cells via Direct Interaction with Cancer-Associated Fibroblasts Promotes Esophageal Squamous Cell Carcinoma Progression Through EGFR-Erk/p38 MAPK Signaling.","authors":"Takashi Nakanishi, Yu-Ichiro Koma, Shoji Miyako, Rikuya Torigoe, Hiroki Yokoo, Masaki Omori, Keitaro Yamanaka, Nobuaki Ishihara, Shuichi Tsukamoto, Takayuki Kodama, Mari Nishio, Manabu Shigeoka, Hiroshi Yokozaki, Yoshihiro Kakeji","doi":"10.3390/cells13201733","DOIUrl":"https://doi.org/10.3390/cells13201733","url":null,"abstract":"<p><p>Cancer-associated fibroblasts (CAFs) are a key component of the tumor microenvironment and significantly contribute to the progression of various cancers, including esophageal squamous cell carcinoma (ESCC). Our previous study established a direct co-culture system of human bone marrow-derived mesenchymal stem cells (progenitors of CAFs) and ESCC cell lines, which facilitates the generation of CAF-like cells and enhances malignancy in ESCC cells. In this study, we further elucidated the mechanism by which CAFs promote ESCC progression using cDNA microarray analysis of monocultured ESCC cells and those co-cultured with CAFs. We observed an increase in the expression and secretion of amphiregulin (AREG) and the expression and phosphorylation of its receptor EGFR in co-cultured ESCC cells. Moreover, AREG treatment of ESCC cells enhanced their survival and migration via the EGFR-Erk/p38 MAPK signaling pathway. Immunohistochemical analysis of human ESCC tissues showed a positive correlation between the intensity of AREG expression at the tumor-invasive front and the expression level of the CAF marker FAP. Bioinformatics analysis confirmed significant upregulation of <i>AREG</i> in ESCC compared with normal tissues. These findings suggest that AREG plays a crucial role in CAF-mediated ESCC progression and could be a novel therapeutic target for ESCC.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"13 20","pages":""},"PeriodicalIF":5.1,"publicationDate":"2024-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11506648/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495911","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}
引用次数: 0
Transplacental Transfer of Oxytocin and Its Impact on Neonatal Cord Blood and In Vitro Retinal Cell Activity. 经胎盘转移催产素及其对新生儿脐带血和体外视网膜细胞活性的影响
IF 5.1 2区 生物学
Cells Pub Date : 2024-10-19 DOI: 10.3390/cells13201735
Claudette O Adegboro, Wenxiang Luo, Meha Kabra, Ryan M McAdams, Nathaniel W York, Ruwandi I Wijenayake, Kiana M Suchla, De-Ann M Pillers, Bikash R Pattnaik
{"title":"Transplacental Transfer of Oxytocin and Its Impact on Neonatal Cord Blood and In Vitro Retinal Cell Activity.","authors":"Claudette O Adegboro, Wenxiang Luo, Meha Kabra, Ryan M McAdams, Nathaniel W York, Ruwandi I Wijenayake, Kiana M Suchla, De-Ann M Pillers, Bikash R Pattnaik","doi":"10.3390/cells13201735","DOIUrl":"https://doi.org/10.3390/cells13201735","url":null,"abstract":"<p><p>The development of fetal organs can be impacted by systemic changes in maternal circulation, with the placenta playing a pivotal role in maintaining pregnancy homeostasis and nutrient exchange. In clinical obstetrics, oxytocin (OXT) is commonly used to induce labor. To explore the potential role of OXT in the placental homeostasis of OXT, we compared OXT levels in neonatal cord blood among neonates (23-42 weeks gestation) whose mothers either received prenatal OXT or experienced spontaneous labor. Our previous research revealed that the oxytocin receptor (OXTR), essential in forming the blood-retina barrier, is expressed in the retinal pigment epithelium (RPE). We hypothesized that perinatal OXT administration might influence the development of the neural retina and its vasculature, offering therapeutic potential for retinal diseases such as retinopathy of prematurity (ROP). Plasma OXT levels were measured using a commercial OXT ELISA kit. Human fetal RPE (hfRPE) cells treated with OXT (10 µM) were assessed for gene expression via RNA sequencing, revealing 14 downregulated and 32 upregulated genes. To validate these differentially expressed genes (DEGs), hfRPE cells were exposed to OXT (0.01, 0.1, 1, or 10 µM) for 12 h, followed by RNA analysis via real-time PCR. Functional, enrichment, and network analyses (Gene Ontology term, FunRich, Cytoscape) were performed to predict the affected pathways. This translational study suggests that OXT likely crosses the placenta, altering fetal OXT concentrations. RNA sequencing identified 46 DEGs involved in vital metabolic and signaling pathways and critical cellular components. Our results indicate that the perinatal administration of OXT may affect neural retina and retinal vessel development, making OXT a potential therapeutic option for developmental eye diseases, including ROP.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"13 20","pages":""},"PeriodicalIF":5.1,"publicationDate":"2024-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11506339/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495971","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}
引用次数: 0
Chicken Embryo Fibroblast Viability and Trans-Differentiation Potential for Cultured Meat Production Across Passages. 鸡胚胎成纤维细胞在不同阶段培养肉类生产中的活力和转分化潜力。
IF 5.1 2区 生物学
Cells Pub Date : 2024-10-19 DOI: 10.3390/cells13201734
So-Hee Kim, Chan-Jin Kim, Eun-Yeong Lee, Young-Hwa Hwang, Seon-Tea Joo
{"title":"Chicken Embryo Fibroblast Viability and Trans-Differentiation Potential for Cultured Meat Production Across Passages.","authors":"So-Hee Kim, Chan-Jin Kim, Eun-Yeong Lee, Young-Hwa Hwang, Seon-Tea Joo","doi":"10.3390/cells13201734","DOIUrl":"https://doi.org/10.3390/cells13201734","url":null,"abstract":"<p><p>This study was conducted to analyze the viability of primary chicken embryo fibroblasts and the efficiency of adipogenic trans-differentiation for cultured meat production. In isolating chicken embryo fibroblasts (CEFs) from a heterogeneous cell pool containing chicken satellite cells (CSCs), over 90% of CEFs expressed CD29 and vimentin. The analysis of the proliferative capabilities of CEFs revealed no significant differences in EdU-positive cells (%), cumulative cell number, doubling time, and growth rate from passage 1 to passage 9 (<i>p</i> > 0.05). This indicates that CEFs can be isolated by 2 h of pre-plating and survive stably up to passage 9, and that primary fibroblasts can serve as a valuable cell source for the cultured meat industry. Adipogenic trans-differentiation was induced up to passage 9 of CEFs. As passages increased, lipid accumulation and adipocyte size significantly decreased (<i>p</i> < 0.05). The reduced differentiation rate of primary CEFs with increasing passages poses a major challenge to the cost and efficiency of cultured meat production. Thus, effective cell management and the maintenance of cellular characteristics for a long time are crucial for ensuring stable and efficient cultured fat production in the cultured meat industry.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"13 20","pages":""},"PeriodicalIF":5.1,"publicationDate":"2024-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11506350/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495930","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}
引用次数: 0
Sex Differences in Astrocyte Activity. 星形胶质细胞活动的性别差异
IF 5.1 2区 生物学
Cells Pub Date : 2024-10-18 DOI: 10.3390/cells13201724
Elisa Gozlan, Yarden Lewit-Cohen, Dan Frenkel
{"title":"Sex Differences in Astrocyte Activity.","authors":"Elisa Gozlan, Yarden Lewit-Cohen, Dan Frenkel","doi":"10.3390/cells13201724","DOIUrl":"https://doi.org/10.3390/cells13201724","url":null,"abstract":"<p><p>Astrocytes are essential for maintaining brain homeostasis. Alterations in their activity have been associated with various brain pathologies. Sex differences were reported to affect astrocyte development and activity, and even susceptibility to different neurodegenerative diseases. This review aims to summarize the current knowledge on the effects of sex on astrocyte activity in health and disease.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"13 20","pages":""},"PeriodicalIF":5.1,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11506538/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495947","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}
引用次数: 0
Multispectral Imaging of Collagen, NAD(P)H and Flavin Autofluorescence in Mesenchymal Stem Cells Undergoing Trilineage Differentiation. 对进行三系分化的间充质干细胞中的胶原、NAD(P)H 和黄素自发荧光进行多光谱成像。
IF 5.1 2区 生物学
Cells Pub Date : 2024-10-18 DOI: 10.3390/cells13201731
Jared M Campbell, Saabah B Mahbub, Ayad G Anwer, Abbas Habibalahi, Stan Gronthos, Sharon Paton, Shane T Grey, Lindsay E Wu, Robert B Gilchrist, Ewa M Goldys
{"title":"Multispectral Imaging of Collagen, NAD(P)H and Flavin Autofluorescence in Mesenchymal Stem Cells Undergoing Trilineage Differentiation.","authors":"Jared M Campbell, Saabah B Mahbub, Ayad G Anwer, Abbas Habibalahi, Stan Gronthos, Sharon Paton, Shane T Grey, Lindsay E Wu, Robert B Gilchrist, Ewa M Goldys","doi":"10.3390/cells13201731","DOIUrl":"https://doi.org/10.3390/cells13201731","url":null,"abstract":"<p><p>Understanding the molecular mechanisms of differentiation is important for regenerative medicine and developmental biology. This study aims to characterise the role of the glycolysis/oxidative phosphorylation balance as a driver of mesenchymal stem cell (MSC) differentiation. Cells were maintained in normal conditions or stimulated towards the MSC trilineage cell types over 21 days. Multispectral imaging of cell autofluorescence was applied as a non-invasive methodology to continuously image cultures in situ. Spectral signals for collagen, NAD(P)H, and flavins were unmixed. MSCs cultured under chondrogenic conditions exhibited increased collagen levels relative to controls. Following osteogenic induction, MSCs showed increased collagen levels relative to controls during the earlier stages of culture; however, control cells increased their collagen levels as they became confluent. MSCs cultured under adipogenic conditions exhibited lower levels of collagen than controls. The redox ratio (RR; NAD(P)H/flavins) immediately decreased during chondrogenesis, with this early effect persisting throughout the culture compared to control cells, which appeared to increase their RR, similar to osteogenesis. Adipogenesis resulted in a small increase in RR on day 2 relative to control cells, followed by a persistent decrease. Chondrogenic and adipogenic differentiation favoured oxidative phosphorylation, whereas osteogenesis and MSC overgrowth resulted in a glycolytic metabolism. Following consideration of these findings, as well as the diverse reports in the literature, it is concluded that neither enhanced oxidative phosphorylation nor glycolysis are fundamental to the canonical modes of differentiation, and researchers should avoid interpreting shifts as indicating differentiation.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"13 20","pages":""},"PeriodicalIF":5.1,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11505937/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495924","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}
引用次数: 0
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