Human Cell最新文献_第10页

The inhibitory effects of Dulaglutide on cellular senescence against high glucose in human retinal endothelial cells 杜拉鲁肽对人视网膜内皮细胞高糖衰老的抑制作用

IF 4.3 3区生物学

Human Cell Pub Date : 2022-05-18 DOI: 10.1007/s13577-022-00703-7

S. Nian, Yajing Mi, Kai Ren, S. Wang, Mingkai Li, Di Yang

引用次数: 4

In memoriam: Yoshihiro Kikuchi (1939–2022) 纪念：菊池义弘（1939–2022）

IF 4.3 3区生物学

Human Cell Pub Date : 2022-05-16 DOI: 10.1007/s13577-022-00722-4

N. Shinomiya, Tsunekazu Kita, H. Kataoka

引用次数: 0

Serum-derived extracellular vesicles mediate Smad4 expression through shuttling microRNA-27a in the progression of laryngeal squamous cell carcinoma 在喉癌的发展过程中，血清源性细胞外囊泡通过穿梭microRNA-27a介导Smad4表达

IF 4.3 3区生物学

Human Cell Pub Date : 2022-05-12 DOI: 10.1007/s13577-022-00712-6

Y. Shuang, Xiao-feng Yao, Jing Liu, J. Niu, Wenyu Guo, Chao Li

引用次数: 2

STK11 overexpression prevents glucocorticoid-induced osteoporosis via activating the AMPK/SIRT1/PGC1α axis STK11过表达通过激活AMPK/SIRT1/PGC1α轴阻止糖皮质激素诱导的骨质疏松症

IF 4.3 3区生物学

Human Cell Pub Date : 2022-05-11 DOI: 10.1007/s13577-022-00704-6

Jiao Xiao, Wenjin Li, Guojuan Li, Jiankai Tan, Na Dong

引用次数: 3

Regulation of osteogenic differentiation by the pro-inflammatory cytokines IL-1β and TNF-α: current conclusions and controversies 促炎因子IL-1β和TNF-α对成骨分化的调控:目前的结论和争议

IF 4.3 3区生物学

Human Cell Pub Date : 2022-05-06 DOI: 10.1007/s13577-022-00711-7

Qingyun Mo, Wei Zhang, Aijing Zhu, L. Backman, Jialin Chen

引用次数: 10

Factors influencing mesenchymal stromal cells in in vitro cellular models to study retinal pigment epithelial cell rescue 间充质细胞的影响因素在体外细胞模型中研究视网膜色素上皮细胞的抢救作用

IF 4.3 3区生物学

Human Cell Pub Date : 2022-05-05 DOI: 10.1007/s13577-022-00705-5

Girish K Srivastava, David Rodriguez-Crespo, Iván Fernández-Bueno, J. Pastor

引用次数: 0

Long non-coding RNA linc00921 suppresses tumorigenesis and epithelial-to-mesenchymal transition of triple-negative breast cancer via targeting miR-9-5p/LZTS2 axis. 长链非编码RNA linc00921通过靶向miR-9-5p/LZTS2轴抑制三阴性乳腺癌的肿瘤发生和上皮-间质转化。

IF 4.3 3区生物学

Human Cell Pub Date : 2022-05-01 Epub Date: 2022-02-18 DOI: 10.1007/s13577-022-00685-6

Jie Zhang, Lina Zhang, Jianlong Wang, Jing Zhao, Xuelian Zhao, Chunli Zhang, Peng Han, Cuizhi Geng

{"title":"Long non-coding RNA linc00921 suppresses tumorigenesis and epithelial-to-mesenchymal transition of triple-negative breast cancer via targeting miR-9-5p/LZTS2 axis.","authors":"Jie Zhang, Lina Zhang, Jianlong Wang, Jing Zhao, Xuelian Zhao, Chunli Zhang, Peng Han, Cuizhi Geng","doi":"10.1007/s13577-022-00685-6","DOIUrl":"https://doi.org/10.1007/s13577-022-00685-6","url":null,"abstract":"Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer. Dysregulation of long non-coding RNAs (lncRNAs) plays crucial roles in the initiation and progression of TNBC. In this study, we analyzed public GEO profiles to verify the key lncRNAs in TNBC. Linc00921 was selected for further study. Low expression of linc00921 was observed in 49 of 95 TNBC tissues. Low expression of linc00921 was correlated with poor postoperative disease-free survival (DFS) and overall survival (OS) of TNBC patients. Overexpression of linc00921 with lentivirus suppressed the proliferation, migration and invasion of TNBC cells. A luciferase reporter assay showed that linc00921 could sponge miR-9-5p in TNBC. Moreover, linc00921 and miR-9-5p occupied the same Argonaute-2 (Ago2) protein in TNBC cells. Leucine zipper tumor suppressor 2 (LZTS2) was recognized as a target gene of miR-9-5p, and thereby a linc00921/miR-9-5p/LZTS2 axis was identified in TNBC cells. Overexpression of linc00921 promoted nuclear export of β-catenin, neutralized its function, and subsequently promoted epithelial-to-mesenchymal transition (EMT) in TNBC. A xenograft tumor mouse model showed that the miR-9-5p inhibitor upregulates LZTS2 expression and induce nuclear export of β-catenin in TNBC. Thus, linc00921 upregulates LZTS2 by sponging miR-9-5p to suppress tumorigenesis and EMT of TNBC. Linc00921/miR-9-5p/LZTS2 axis may be a novel biomarker and therapeutic target for TNBC patients.","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 3","pages":"909-923"},"PeriodicalIF":4.3,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9013323/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39934636","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: 4

A20 alleviated caspase-1-mediated pyroptosis and inflammation stimulated by Porphyromonas gingivalis lipopolysaccharide and nicotine through autophagy enhancement. A20通过增强自噬来减轻由牙龈卟啉单胞菌脂多糖和尼古丁引起的caspase-1介导的焦亡和炎症。

IF 4.3 3区生物学

Human Cell Pub Date : 2022-05-01 Epub Date: 2022-02-25 DOI: 10.1007/s13577-022-00678-5

Hui Tang, Yu Ye, Lu Li, Yi Zhou, Liguang Hou, Shuangshuang Ren, Yan Xu

{"title":"A20 alleviated caspase-1-mediated pyroptosis and inflammation stimulated by Porphyromonas gingivalis lipopolysaccharide and nicotine through autophagy enhancement.","authors":"Hui Tang, Yu Ye, Lu Li, Yi Zhou, Liguang Hou, Shuangshuang Ren, Yan Xu","doi":"10.1007/s13577-022-00678-5","DOIUrl":"https://doi.org/10.1007/s13577-022-00678-5","url":null,"abstract":"Periodontitis is the leading cause of tooth loss, and patients with smoking habits are at an increased risk of developing periodontitis. A20 (the tumor necrosis factor alpha-induced protein 3, TNFAIP3) is one of the key regulators of inflammation and cell death in numerous tissues. Emerging researches indicated A20 as a fundamental molecule in the periodontal tissue. This study was to evaluate the role of A20 against cell death and inflammation in periodontitis and to elucidate the underlying mechanisms. In our study, western blot, autophagy detection, and transmission electron microscopy showed that lipopolysaccharide from Porphyromonas gingivalis (Pg.LPS) and nicotine (NI) could enhance the activation of autophagy. Pg.LPS and NI induce the pyroptosis of human periodontal ligament cells (hPDLCs), as evidenced by the decrease of membrane integrity and the increase of NLRP3, GSDMD, GSDMD-N, caspase-1 activity, and the pro-inflammatory cytokines of IL-1β, IL-6, TNF-α. Further researches were focused on that A20, an ubiquitin-editing enzyme, was linked to hPDLCs pyroptosis. Overexpression or silencing A20 could diminish or aggravate pyroptosis in hPDLCs by the modulation of autophagy. The above results demonstrated that A20 dictated the cross-talk between pyroptosis and autophagy. Overexpression of A20 enhanced autophagy to reduce pyroptosis, and thus alleviating inflammation, suggesting that A20 may be a potent target in the treatment of periodontitis.","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 3","pages":"803-816"},"PeriodicalIF":4.3,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39821600","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: 10

Exosomes derived from bone mesenchymal stem cells attenuate myocardial fibrosis both in vivo and in vitro via autophagy activation: the key role of miR-199a-3p/mTOR pathway. 来源于骨间充质干细胞的外泌体通过自噬激活在体内和体外减弱心肌纤维化:miR-199a-3p/mTOR通路的关键作用。

IF 4.3 3区生物学

Human Cell Pub Date : 2022-05-01 Epub Date: 2022-02-21 DOI: 10.1007/s13577-022-00680-x

Chenrong Fan, Qizeng Wang, Youjin Chen, Tingting Ye, Yuncao Fan

{"title":"Exosomes derived from bone mesenchymal stem cells attenuate myocardial fibrosis both in vivo and in vitro via autophagy activation: the key role of miR-199a-3p/mTOR pathway.","authors":"Chenrong Fan, Qizeng Wang, Youjin Chen, Tingting Ye, Yuncao Fan","doi":"10.1007/s13577-022-00680-x","DOIUrl":"https://doi.org/10.1007/s13577-022-00680-x","url":null,"abstract":"Autophagy suppression plays key a role during myocardial fibrosis (MF) progression. Exosomes from stem cells attenuate MF. The current study aimed to explain the antifibrosis effects of exosomes by focusing on microRNAs (miRs). MF was induced in rats using transverse aortic constriction (TAC) method and handled with exosomes from bone mesenchymal stem cells (BMSCs). The results of in vivo assays were verified with H9c2 cells. MiR expression profile was determined using microarray detection. The influence of miR-199a-3p modulation in vivo and in vitro on the antifibrosis effect of exosomes then was assessed. Exosomes attenuated MF by inhibiting inflammation, improving tissue structure, and inhibiting fibrosis-related indicators in TAC rats, and the effects were associated with autophagy activation. In H9c2 cells, exosomes suppressed cell viability, induced cell apoptosis, inhibited fibrosis-related indicators, while and the inhibition of autophagy by 3-MA would block the effect of exosomes. Based on the microarray detection, miR-199a-3p level was selected as therapeutic target. The inhibition of miR-199a-3p impaired the antifibrosis effects of exosomes on H9c2 cells, which was associated with autophagy inhibition. Collectively, exosomes from BMSCs exerted antifibrosis effects via the distant transfer of miR-199a-3p to heart tissues, which induced autophagy by inhibiting mTOR.","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 3","pages":"817-835"},"PeriodicalIF":4.3,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39639682","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: 5

Knockout of GGPPS1 restrains rab37-mediated autophagy in response to ventilator-induced lung injury. 敲除 GGPPS1 可抑制 rab37 介导的自噬，以应对呼吸机诱发的肺损伤。

IF 4.3 3区生物学

Human Cell Pub Date : 2022-05-01 Epub Date: 2022-03-25 DOI: 10.1007/s13577-022-00692-7

Zexu Wang, Meizi Chen, Xia Pan, Li Wang, Cheng Yin, Qiuqi Lin, Jingjing Jiang, Yunlei Zhang, Bing Wan

{"title":"Knockout of GGPPS1 restrains rab37-mediated autophagy in response to ventilator-induced lung injury.","authors":"Zexu Wang, Meizi Chen, Xia Pan, Li Wang, Cheng Yin, Qiuqi Lin, Jingjing Jiang, Yunlei Zhang, Bing Wan","doi":"10.1007/s13577-022-00692-7","DOIUrl":"10.1007/s13577-022-00692-7","url":null,"abstract":"Mechanical ventilation may cause ventilator-induced lung injury (VILI) in patients requiring ventilator support. Inhibition of autophagy is an important approach to ameliorate VILI as it always enhances lung injury after exposure to various stress agents. This study aimed to further reveal the potential mechanisms underlying the effects of geranylgeranyl diphosphate synthase large subunit 1 (GGPPS1) knockout and autophagy in VILI using C57BL/6 mice with lung-specific GGPPS1 knockout that were subjected to mechanical ventilation. The results demonstrate that GGPPS1 knockout mice exhibit significantly attenuated VILI based on the histologic score, the lung wet-to-dry ratio, total protein levels, neutrophils in bronchoalveolar lavage fluid, and reduced levels of inflammatory cytokines. Importantly, the expression levels of autophagy markers were obviously decreased in GGPPS1 knockout mice compared with wild-type mice. The inhibitory effects of GGPPS1 knockout on autophagy were further confirmed by measuring the ultrastructural change of lung tissues under transmission electron microscopy. In addition, knockdown of GGPPS1 in RAW264.7 cells reduced cyclic stretch-induced inflammation and autophagy. The benefits of GGPPS1 knockout for VILI can be partially eliminated through treatment with rapamycin. Further analysis revealed that Rab37 was significantly downregulated in GGPPS1 knockout mice after mechanical ventilation, while it was highly expressed in the control group. Simultaneously, Rab37 overexpression significantly enhances autophagy in cells that are treated with cyclin stretch, including GGPPS1 knockout cells. Collectively, our results indicate that GGPPS1 knockout results in reduced expression of Rab37 proteins, further restraining autophagy and VILI.","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":" ","pages":"871-884"},"PeriodicalIF":4.3,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8948466/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40327326","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