Human Cell最新文献_第8页

Crosstalk among proximal tubular cells, macrophages, and fibroblasts in acute kidney injury: single-cell profiling from the perspective of ferroptosis. 急性肾损伤中近端肾小管细胞、巨噬细胞和成纤维细胞之间的相互影响：从铁变态反应的角度进行单细胞特征分析。

IF 3.4 3区生物学

Human Cell Pub Date : 2024-07-01 Epub Date: 2024-05-16 DOI: 10.1007/s13577-024-01072-z

Yulin Wang, Ziyan Shen, Shaocong Mo, Han Zhang, Jing Chen, Cheng Zhu, Shiqi Lv, Di Zhang, Xinhui Huang, Yulu Gu, Xixi Yu, Xiaoqiang Ding, Xiaoyan Zhang

{"title":"Crosstalk among proximal tubular cells, macrophages, and fibroblasts in acute kidney injury: single-cell profiling from the perspective of ferroptosis.","authors":"Yulin Wang, Ziyan Shen, Shaocong Mo, Han Zhang, Jing Chen, Cheng Zhu, Shiqi Lv, Di Zhang, Xinhui Huang, Yulu Gu, Xixi Yu, Xiaoqiang Ding, Xiaoyan Zhang","doi":"10.1007/s13577-024-01072-z","DOIUrl":"10.1007/s13577-024-01072-z","url":null,"abstract":"The link between ferroptosis, a form of cell death mediated by iron and acute kidney injury (AKI) is recently gaining widespread attention. However, the mechanism of the crosstalk between cells in the pathogenesis and progression of acute kidney injury remains unexplored. In our research, we performed a non-negative matrix decomposition (NMF) algorithm on acute kidney injury single-cell RNA sequencing data based specifically focusing in ferroptosis-associated genes. Through a combination with pseudo-time analysis, cell-cell interaction analysis and SCENIC analysis, we discovered that proximal tubular cells, macrophages, and fibroblasts all showed associations with ferroptosis in different pathways and at various time. This involvement influenced cellular functions, enhancing cellular communication and activating multiple transcription factors. In addition, analyzing bulk expression profiles and marker genes of newly defined ferroptosis subtypes of cells, we have identified crucial cell subtypes, including Egr1 + PTC-C1, Jun + PTC-C3, Cxcl2 + Mac-C1 and Egr1 + Fib-C1. All these subtypes which were found in AKI mice kidneys and played significantly distinct roles from those of normal mice. Moreover, we verified the differential expression of Egr1, Jun, and Cxcl2 in the IRI mouse model and acute kidney injury human samples. Finally, our research presented a novel analysis of the crosstalk of proximal tubular cells, macrophages and fibroblasts in acute kidney injury targeting ferroptosis, therefore, contributing to better understanding the acute kidney injury pathogenesis, self-repairment and acute kidney injury-chronic kidney disease (AKI-CKD) progression.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11194220/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140946360","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

Immunosuppressive regulatory cells in cancer immunotherapy: restrain or modulate? 癌症免疫疗法中的免疫抑制调节细胞：抑制还是调节？

IF 3.4 3区生物学

Human Cell Pub Date : 2024-07-01 Epub Date: 2024-05-30 DOI: 10.1007/s13577-024-01083-w

Yan Wu, Dongfeng Chen, Yang Gao, Qinggang Xu, Yang Zhou, Zhong Ni, Manli Na

引用次数: 0

Developing more comprehensive thyroid cancer organoids for precision medicine. 为精准医疗开发更全面的甲状腺癌器官组织。

IF 3.4 3区生物学

Human Cell Pub Date : 2024-07-01 Epub Date: 2024-04-30 DOI: 10.1007/s13577-024-01070-1

Huihui Yang, Dong Chen

引用次数: 0

Biochemical characterization of renal hypouricemia-associated mutations in urate transporter genes using human cells. 利用人体细胞对肾脏高尿酸血症相关尿酸盐转运体基因突变进行生化鉴定。

IF 3.4 3区生物学

Human Cell Pub Date : 2024-07-01 Epub Date: 2024-05-29 DOI: 10.1007/s13577-024-01079-6

Yu Toyoda, Tappei Takada, Akiyoshi Nakayama, Nariyoshi Shinomiya, Hirotaka Matsuo

引用次数: 0

Identification of a family with van der Hoeve's syndrome harboring a novel COL1A1 mutation and generation of patient-derived iPSC lines and CRISPR/Cas9-corrected isogenic iPSCs. 确定一个携带新型 COL1A1 突变的范德胡夫综合征家族，并生成源自患者的 iPSC 株系和经 CRISPR/Cas9 校正的同源 iPSC。

IF 4.3 3区生物学

Human Cell Pub Date : 2024-05-01 Epub Date: 2024-02-20 DOI: 10.1007/s13577-024-01028-3

SiJun Li, Lingyun Mei, Chufeng He, Xinzhang Cai, Hong Wu, XueWen Wu, Yalan Liu, Yong Feng, Jian Song

{"title":"Identification of a family with van der Hoeve's syndrome harboring a novel COL1A1 mutation and generation of patient-derived iPSC lines and CRISPR/Cas9-corrected isogenic iPSCs.","authors":"SiJun Li, Lingyun Mei, Chufeng He, Xinzhang Cai, Hong Wu, XueWen Wu, Yalan Liu, Yong Feng, Jian Song","doi":"10.1007/s13577-024-01028-3","DOIUrl":"10.1007/s13577-024-01028-3","url":null,"abstract":"Van der Hoeve's syndrome, also known as osteogenesis imperfecta (OI), is a genetic connective tissue disorder characterized by fragile, fracture-prone bone and hearing loss. The disease is caused by a gene mutation in one of the two type I collagen genes COL1A1 or COL1A2. In this study, we identified a novel frameshift mutation of the COL1A1 gene (c.1607delG) in a family with OI using whole-exome sequencing, bioinformatics analysis and Sanger sequencing. This mutation may lead to the deletion of a portion of exon 23 and the generation of a premature stop codon in the COL1A1 gene. To further investigate the impact of this mutation, we established two induced pluripotent stem cell (iPSC) lines from peripheral blood mononuclear cells of OI patients carrying a novel mutation in the COL1A1 gene. Osteoblasts (OB) derived from OI-iPSCs exhibited reduced production of type I collagen and diminished ability to differentiate into osteoblasts. Using a CRISPR-based homology-directed repair strategy, we corrected the OI disease-causing COL1A1 novel mutations in iPSCs generated from an affected individual. Our results demonstrated that the diminished expression of type I collagen and osteogenic potential were enhanced in OB induced from corrected OI-iPSCs compared to those from OI-iPSCs. Overall, our results provide new insights into the genetic basis of Van der Hoeve's syndrome and highlight the potential of iPSC technology for disease modeling and therapeutic development.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":null,"pages":null},"PeriodicalIF":4.3,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139913888","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

Liraglutide prevents cellular senescence in human retinal endothelial cells (HRECs) mediated by SIRT1: an implication in diabetes retinopathy. 利拉鲁肽通过 SIRT1 阻止人视网膜内皮细胞（HRECs）的细胞衰老：与糖尿病视网膜病变有关。

IF 4.3 3区生物学

Human Cell Pub Date : 2024-05-01 Epub Date: 2024-03-04 DOI: 10.1007/s13577-024-01038-1

Lihua Hou, Jianying Du, Yongxiao Dong, Min Wang, Libo Wang, Jifei Zhao

{"title":"Liraglutide prevents cellular senescence in human retinal endothelial cells (HRECs) mediated by SIRT1: an implication in diabetes retinopathy.","authors":"Lihua Hou, Jianying Du, Yongxiao Dong, Min Wang, Libo Wang, Jifei Zhao","doi":"10.1007/s13577-024-01038-1","DOIUrl":"10.1007/s13577-024-01038-1","url":null,"abstract":"Diabetes mellitus (DM) is a chronic metabolic disorder affecting millions of people worldwide, characterized by dysregulated glucose homeostasis and hyperglycemia. Diabetic retinopathy (DR) is one of the serious multisystemic complications. Aging is an important risk factor for DR. Endothelial sirtuin 1 (SIRT1) plays an important role in regulating the pathophysiology of glucose metabolism, cellular senescence, and aging. Liraglutide, an analog of Glucagon-like peptide 1 (GLP-1), has been widely used in the treatment of DM. However, the effects of Liraglutide on DR are less reported. Here, we investigated whether treatment with Liraglutide has beneficial effects on high glucose (HG)-induced injury in human retinal microvascular endothelial cells (HRECs). First, we found that exposure to HG reduced the expression of glucagon-like peptide 1 receptor 1 (GLP-1R). Additionally, Liraglutide ameliorated HG-induced increase in the expression of vascular endothelial growth factor-A (VEGF-A) and interleukin 6 (IL-6). Importantly, Liraglutide ameliorated cellular senescence and increased telomerase activity in HG-challenged HRECs. Liraglutide also reduced the levels of p53 and p21. Mechanistically, Liraglutide restored the expression of SIRT1 against HG. In contrast, the knockdown of SIRT1 abolished the protective effects of Liraglutide in cellular senescence of HRECs. Our findings suggest that Liraglutide might possess a benefit on DR mediated by SIRT1.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":null,"pages":null},"PeriodicalIF":4.3,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11016519/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140029383","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

Anexelekto (AXL) no more: microRNA-155 (miR-155) controls the "Uncontrolled" in SARS-CoV-2. 不再有 Anexelekto (AXL)：microRNA-155 (miR-155) 控制着 SARS-CoV-2 中的 "失控"。

IF 4.3 3区生物学

Human Cell Pub Date : 2024-05-01 Epub Date: 2024-03-12 DOI: 10.1007/s13577-024-01041-6

K I Papadopoulos, A Papadopoulou, T C Aw

{"title":"Anexelekto (AXL) no more: microRNA-155 (miR-155) controls the \"Uncontrolled\" in SARS-CoV-2.","authors":"K I Papadopoulos, A Papadopoulou, T C Aw","doi":"10.1007/s13577-024-01041-6","DOIUrl":"10.1007/s13577-024-01041-6","url":null,"abstract":"AXL is the gene that encodes the Anexelekto (AXL) receptor tyrosine kinase that demonstrates significant roles in various cellular processes, including cell growth, survival, and migration. Anexelekto is a Greek word meaning excessive and uncontrolled, semantically implying the crucial involvement of AXL in cancer and immune biology, and in promoting cancer metastasis. AXL overexpression appears to drive epithelial to mesenchymal transition, tumor angiogenesis, decreased antitumor immune response, and resistance to therapeutic agents. Recently, AXL has been reported to play important roles in several viral infections, including SARS-CoV-2. We have previously outlined the importance of microRNAs (miRNAs, miRs) and especially miR-155 in SARS-CoV-2 pathophysiology through regulation of the Renin-Angiotensin Aldosterone System (RAAS) and influence on several aspects of host innate immunity. MiRNAs are negative regulators of gene expression, decreasing the stability of target RNAs or limiting their translation and, enthrallingly, miR-155 is also involved in AXL homeostasis-both endogenously and pharmaceutically using repurposed drugs (e.g., metformin)-highlighting thrifty evolutionary host innate immunity mechanisms that successfully can thwart viral entry and replication. Cancer, infections, and immune system disturbances will increasingly involve miRNA diagnostics and therapeutics in the future.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":null,"pages":null},"PeriodicalIF":4.3,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140111875","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

Knockdown of nicotinamide N-methyltransferase suppresses proliferation, migration, and chemoresistance of Merkel cell carcinoma cells in vitro. 敲除烟酰胺 N-甲基转移酶可抑制梅克尔细胞癌细胞在体外的增殖、迁移和化疗抗性。

IF 4.3 3区生物学

Human Cell Pub Date : 2024-05-01 Epub Date: 2024-03-19 DOI: 10.1007/s13577-024-01047-0

Valentina Pozzi, Elisa Molinelli, Roberto Campagna, Emma N Serritelli, Monia Cecati, Edoardo De Simoni, Davide Sartini, Gaia Goteri, Nathaniel I Martin, Matthijs J van Haren, Eleonora Salvolini, Oriana Simonetti, Annamaria Offidani, Monica Emanuelli

{"title":"Knockdown of nicotinamide N-methyltransferase suppresses proliferation, migration, and chemoresistance of Merkel cell carcinoma cells in vitro.","authors":"Valentina Pozzi, Elisa Molinelli, Roberto Campagna, Emma N Serritelli, Monia Cecati, Edoardo De Simoni, Davide Sartini, Gaia Goteri, Nathaniel I Martin, Matthijs J van Haren, Eleonora Salvolini, Oriana Simonetti, Annamaria Offidani, Monica Emanuelli","doi":"10.1007/s13577-024-01047-0","DOIUrl":"10.1007/s13577-024-01047-0","url":null,"abstract":"Merkel cell carcinoma (MCC) is an aggressive skin cancer, with a propensity for early metastasis. Therefore, early diagnosis and the identification of novel targets become fundamental. The enzyme nicotinamide N-methyltransferase (NNMT) catalyzes the reaction of N-methylation of nicotinamide and other analogous compounds. Although NNMT overexpression was reported in many malignancies, the significance of its dysregulation in cancer cell phenotype was partly clarified. Several works demonstrated that NNMT promotes cancer cell proliferation, migration, and chemoresistance. In this study, we investigated the possible involvement of this enzyme in MCC. Preliminary immunohistochemical analyses were performed to evaluate NNMT expression in MCC tissue specimens. To explore the enzyme function in tumor cell metabolism, MCC cell lines have been transfected with plasmids encoding for short hairpin RNAs (shRNAs) targeting NNMT mRNA. Preliminary immunohistochemical analyses showed elevated NNMT expression in MCC tissue specimens. The effect of enzyme downregulation on cell proliferation, migration, and chemosensitivity was then evaluated through MTT, trypan blue, and wound healing assays. Data obtained clearly demonstrated that NNMT knockdown is associated with a decrease of cell proliferation, viability, and migration, as well as with enhanced sensitivity to treatment with chemotherapeutic drugs. Taken together, these results suggest that NNMT could represent an interesting MCC biomarker and a promising target for targeted anti-cancer therapy.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":null,"pages":null},"PeriodicalIF":4.3,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11016511/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140177347","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

Prognostic value of inflammation and immune-related gene NOD2 in clear cell renal cell carcinoma. 透明细胞肾细胞癌中炎症和免疫相关基因 NOD2 的预后价值。

IF 4.3 3区生物学

Human Cell Pub Date : 2024-05-01 Epub Date: 2024-03-21 DOI: 10.1007/s13577-024-01045-2

Lei Lyu, Rui Min, Fuxin Zheng, Wei Xiang, Tao Huang, Yan Feng, Chuanhua Zhang, Jingdong Yuan

{"title":"Prognostic value of inflammation and immune-related gene NOD2 in clear cell renal cell carcinoma.","authors":"Lei Lyu, Rui Min, Fuxin Zheng, Wei Xiang, Tao Huang, Yan Feng, Chuanhua Zhang, Jingdong Yuan","doi":"10.1007/s13577-024-01045-2","DOIUrl":"10.1007/s13577-024-01045-2","url":null,"abstract":"Inflammation and immune responses play important roles in cancer development and prognosis. We identified 59 upregulated inflammation- and immune-related genes (IIRGs) in clear cell renal cell carcinoma (ccRCC) from The Cancer Genome Atlas database. Among the upregulated IIRGs, nucleotide binding oligomerization domain 2 (NOD2), PYD and CARD domain (PYCARD) were also confirmed to be upregulated in the Oncomine database and in three independent GEO data sets. Tumor immune infiltration resource database analysis revealed that NOD2 and PYCARD levels were significantly positively correlated with infiltration levels of B cells, CD4+ T cells, CD8+ T cells, neutrophils, macrophages and dendritic cells. Multivariate Cox hazards regression analysis indicated that based on clinical variables (age, gender, tumor grade, pathological TNM stage), NOD2, but not PYCARD, was an independent, unfavorable ccRCC prognostic biomarker. Functional enrichment analyses (GSEA) showed that NOD2 was involved in innate immune responses, inflammatory responses, and regulation of cytokine secretion. Meanwhile, mRNA and protein levels of NOD2 were elevated in four ccRCC cell lines (786-O, ACHN, A498 and Caki-1), and its knockdown significantly inhibited IL-8 secretion, thereby inhibiting ccRCC cell proliferation and invasion. Furthermore, results showed that miR-20b-5p targeted NOD2 to alleviate NOD2-mediated IL-8 secretion. In conclusion, NOD2 is a potential prognostic biomarker for ccRCC and the miR-20b-5p/NOD2/IL-8 axis may regulate inflammation- and immune-mediated tumorigenesis in ccRCC.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":null,"pages":null},"PeriodicalIF":4.3,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140177348","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

Lactate in breast cancer cells is associated with evasion of hypoxia-induced cell cycle arrest and adverse patient outcome. 乳腺癌细胞中的乳酸与逃避缺氧诱导的细胞周期停滞和患者的不良预后有关。

IF 3.4 3区生物学

Human Cell Pub Date : 2024-05-01 Epub Date: 2024-03-13 DOI: 10.1007/s13577-024-01046-1

Yamin Liu, Yasir Suhail, Ashkan Novin, Junaid Afzal, Aditya Pant, Kshitiz

{"title":"Lactate in breast cancer cells is associated with evasion of hypoxia-induced cell cycle arrest and adverse patient outcome.","authors":"Yamin Liu, Yasir Suhail, Ashkan Novin, Junaid Afzal, Aditya Pant, Kshitiz","doi":"10.1007/s13577-024-01046-1","DOIUrl":"10.1007/s13577-024-01046-1","url":null,"abstract":"Tumor hypoxia is a common microenvironmental factor in breast cancers, resulting in stabilization of Hypoxia-Inducible Factor 1 (HIF-1), the master regulator of hypoxic response in cells. Metabolic adaptation by HIF-1 results in inhibition of citric acid cycle, causing accumulation of lactate in large concentrations in hypoxic cancers. Lactate can therefore serve as a secondary microenvironmental factor influencing cellular response to hypoxia. Presence of lactate can alter the hypoxic response of breast cancers in many ways, sometimes in opposite manners. Lactate stabilizes HIF-1 in oxidative condition, as well as destabilizes HIF-1 in hypoxia, increases cellular acidification, and mitigates HIF-1-driven inhibition of cellular respiration. We therefore tested the effect of lactate in MDA-MB-231 under hypoxia, finding that lactate can activate pathways associated with DNA replication, and cell cycling, as well as tissue morphogenesis associated with invasive processes. Using a bioengineered nano-patterned stromal invasion assay, we also confirmed that high lactate and induced HIF-1α gene overexpression can synergistically promote MDA-MB-231 dissemination and stromal trespass. Furthermore, using The Cancer Genome Atlas, we also surprisingly found that lactate in hypoxia promotes gene expression signatures prognosticating low survival in breast cancer patients. Our work documents that lactate accumulation contributes to increased heterogeneity in breast cancer gene expression promoting cancer growth and reducing patient survival.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11256967/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140121174","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