Human Cell最新文献_第4页

SRGAP2 controls colorectal cancer chemosensitivity via regulation of mitochondrial complex I activity. SRGAP2通过调节线粒体复合体I活性来控制结直肠癌的化疗敏感性。

IF 4.3 3区生物学

Human Cell Pub Date : 2022-11-01 Epub Date: 2022-09-05 DOI: 10.1007/s13577-022-00781-7

Yongqin Tang, Guijun Liu, Yanhan Jia, Tao Sun

引用次数: 1

Restoration of vascular endothelial integrity by mesenchymal stromal/stem cells in debilitating virus diseases. 间充质基质/干细胞在衰弱性病毒疾病中的血管内皮完整性修复

IF 4.3 3区生物学

Human Cell Pub Date : 2022-11-01 Epub Date: 2022-09-06 DOI: 10.1007/s13577-022-00785-3

Agieshkumar Balakrishna Pillai, Vignesh Mariappan, Aashika Raagavi JeanPierre, S R Rao

{"title":"Restoration of vascular endothelial integrity by mesenchymal stromal/stem cells in debilitating virus diseases.","authors":"Agieshkumar Balakrishna Pillai, Vignesh Mariappan, Aashika Raagavi JeanPierre, S R Rao","doi":"10.1007/s13577-022-00785-3","DOIUrl":"https://doi.org/10.1007/s13577-022-00785-3","url":null,"abstract":"Endothelial dysfunction is one of the key cornerstone complications of emerging and re-emerging viruses which lead to vascular leakage and a high mortality rate. The mechanism that regulates the origin of endothelial dysregulation is not completely elucidated. Currently, there are no potential pharmacological treatments and curable management for such diseases. In this sense, mesenchymal stromal/stem cells (MSCs) has been emerging to be a promising therapeutic strategy in restoring endothelial barrier function in various lung disease, including ALI and ARDS. The mechanism of the role of MSCs in restoring endothelial integrity among single-strand RNA (ssRNA) viruses that target endothelial cells remains elusive. Thus, we have discussed the therapeutic role of MSCs in restoring vascular integrity by (i) inhibiting the metalloprotease activity thereby preventing the cleavage of tight junction proteins, which are essential for maintaining membrane integrity (ii) possessing antioxidant properties which neutralize the excessive ROS production due to virus infection and its associated hyper host immune response (iii) modulating micro RNAs that regulate the endothelial activation and its integrity by downregulating the inflammatory response during ssRNA infection.","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 6","pages":"1633-1639"},"PeriodicalIF":4.3,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9447969/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40353550","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: 2

S1P-S1PR1 signaling switch: a new paradigm of tyrosine phosphorylation. S1P-S1PR1信号开关:酪氨酸磷酸化的新范式。

IF 4.3 3区生物学

Human Cell Pub Date : 2022-11-01 Epub Date: 2022-09-03 DOI: 10.1007/s13577-022-00783-5

Zeeshan Z Banday

引用次数: 0

ELK1 suppresses SYTL1 expression by recruiting HDAC2 in bladder cancer progression. ELK1在膀胱癌进展中通过募集HDAC2抑制SYTL1表达。

IF 4.3 3区生物学

Human Cell Pub Date : 2022-11-01 Epub Date: 2022-09-15 DOI: 10.1007/s13577-022-00789-z

Jiansong Wang, Jianjun Luo, Xuecheng Wu, Zhuo Li

引用次数: 0

Establishment and characterization of NCC-MFS6-C1: a novel patient-derived cell line of myxofibrosarcoma. NCC-MFS6-C1:一种新的黏液纤维肉瘤患者来源细胞系的建立和表征。

IF 4.3 3区生物学

Human Cell Pub Date : 2022-11-01 Epub Date: 2022-08-10 DOI: 10.1007/s13577-022-00749-7

Yuki Yoshimatsu, Rei Noguchi, Yooksil Sin, Ryuto Tsuchiya, Takuya Ono, Taro Akiyama, Chiaki Sato, Eisuke Kobayashi, Naoki Kojima, Akihiko Yoshida, Akira Kawai, Tadashi Kondo

{"title":"Establishment and characterization of NCC-MFS6-C1: a novel patient-derived cell line of myxofibrosarcoma.","authors":"Yuki Yoshimatsu, Rei Noguchi, Yooksil Sin, Ryuto Tsuchiya, Takuya Ono, Taro Akiyama, Chiaki Sato, Eisuke Kobayashi, Naoki Kojima, Akihiko Yoshida, Akira Kawai, Tadashi Kondo","doi":"10.1007/s13577-022-00749-7","DOIUrl":"https://doi.org/10.1007/s13577-022-00749-7","url":null,"abstract":"Myxofibrosarcoma (MFS) is a rare and aggressive mesenchymal malignancy characterized by complex karyotypes with heterogeneous clinical features. The standard treatment for primary MFS is curative resection; however, the utility of systemic chemotherapy and radiotherapy has not been established. Although patient-derived cancer cell lines are a key bioresource for developing novel therapies, the number of MFS cell lines available from public cell banks is limited by the rarity of the disease, and large-scale drug screening has not yet been performed. To address this issue, we aimed to establish and characterize a novel MFS cell line. We successfully established a cell line, NCC-MFS6-C1, which harbors genetic abnormalities common in MFS and exhibits aggressive phenotypes such as continuous growth, spheroid formation, and invasion in tissue culture conditions. We performed drug screening using NCC-MFS6-C1 along with five MFS cell lines established in our laboratory and clarified the response spectrum of 214 existing anticancer agents. We found that two anticancer agents, gemcitabine and romidepsin, showed considerable antiproliferative effects, and these observations were concordant with the findings of our previous report, in which these agents attenuated the proliferation of five previously reported MFS cell lines. We conclude that NCC-MFS6-C1 is a useful resource for studying MFS.","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 6","pages":"1993-2001"},"PeriodicalIF":4.3,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40683221","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

SQSTM1/p62 promotes miR-198 loading into extracellular vesicles and its autophagy-related secretion. SQSTM1/p62促进miR-198装载到细胞外囊泡及其自噬相关的分泌。

IF 4.3 3区生物学

Human Cell Pub Date : 2022-11-01 Epub Date: 2022-09-01 DOI: 10.1007/s13577-022-00765-7

Xiaojie Yu, Hannah Eischeid-Scholz, Lydia Meder, Vangelis Kondylis, Reinhard Büttner, Margarete Odenthal

{"title":"SQSTM1/p62 promotes miR-198 loading into extracellular vesicles and its autophagy-related secretion.","authors":"Xiaojie Yu, Hannah Eischeid-Scholz, Lydia Meder, Vangelis Kondylis, Reinhard Büttner, Margarete Odenthal","doi":"10.1007/s13577-022-00765-7","DOIUrl":"https://doi.org/10.1007/s13577-022-00765-7","url":null,"abstract":"MicroRNA dysregulation is a hallmark of hepatocellular carcinoma (HCC), leading to tumor growth and metastasis. Previous screening on patient specimens identified miR-198 as the most downregulated miRNA in HCC. Here, we show that miR-198 compensation leads to self-release into extracellular vesicles (EVs). Importantly, the vesicular secretion is mediated by autophagy-related pathway, initiated by sequestration of p62/miR-198 complexes in autophagosome-associated vesicle fractions. miR-198 is selectively recognized and loaded by p62 into autophagosomal fractions, whereas mutated miR-198 forms neither induce autophagy and nor interact with p62. Gain and loss of function experiments, using a CRIPR/Cas knockout (KO) and transgenic site-specific p62 mutants, identified p62 as an essential repressor of cellular miR-198 abundancy. Notably, EVs, harboring miR-198/p62 protein complexes, can be uptaken by cells in the close vicinity, leading to change of gene expression in recipient cells. In conclusion, miR-198 enhances autophagy; conversely autophagic protein p62 reduces the miR-198 levels by sorting into extracellular space. miR-198 is at first transcribed as primary miRNA, after being processed into single stranded mature miR-198 form, it is transported into cytoplasm ①. By interaction with p62 protein, miR-198 conglomerates and forms a binding complex ②. Since LC3 protein is an interaction partner of p62 protein, hence miR-198 is included into autophagosomes ③. By fusion with multivesicular bodies (MVB), miR-198-binding complex was recruited into amphisomes ④, the latter of which quickly turns into secretory MVB containing intraluminal vesicles⑤. By fusion with cell membrane, intraluminal vesicles were released into extracellular space as EVs ⑥.","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 6","pages":"1766-1784"},"PeriodicalIF":4.3,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9515045/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40340537","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: 1

Retraction Note to: 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. 注:骨间充质干细胞衍生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 : 2022-11-01 DOI: 10.1007/s13577-022-00761-x

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

引用次数: 0

FOSL2 deficiency delays nonalcoholic steatohepatitis progression by regulating LY6D-mediated NLRP3 activation. FOSL2缺乏通过调节ly6d介导的NLRP3激活来延缓非酒精性脂肪性肝炎的进展。

IF 4.3 3区生物学

Human Cell Pub Date : 2022-11-01 Epub Date: 2022-08-05 DOI: 10.1007/s13577-022-00760-y

Pei-Xin Hu, Mei-Yan Sheng, Yan-Ping Liu, Chun-Qing Zhang

{"title":"FOSL2 deficiency delays nonalcoholic steatohepatitis progression by regulating LY6D-mediated NLRP3 activation.","authors":"Pei-Xin Hu, Mei-Yan Sheng, Yan-Ping Liu, Chun-Qing Zhang","doi":"10.1007/s13577-022-00760-y","DOIUrl":"https://doi.org/10.1007/s13577-022-00760-y","url":null,"abstract":"Lymphocyte antigen 6 family member D (LY6D) was enhanced specifically in senescent cells, while its effects on pyroptosis, a programmed cell death, remains unknown. The goal of this study was to assess the role of LY6D in the mediation of pyroptosis during nonalcoholic steatohepatitis (NASH). After screening out LY6D as a specific liver fibrosis-associated gene using the GSE55747 dataset from the GEO database, we established a NASH mouse model using methionine and choline deficient-diet feeding and an in vitro model using lipopolysaccharide (LPS)-treated hepatocytes. LY6D was overexpressed in NASH livers as well as in LPS-treated hepatocytes. Silencing of LY6D inhibited NASH-associated hepatocyte pyroptosis. With the aid of bioinformatics analysis, promoter-luciferase reporter and ChIP-qPCR assays, we identified FOSL2 as an upstream transcription factor of LY6D. FOSL2, which was highly expressed in NASH, promoted LY6D transcription by binding to the promoter of LY6D. Depletion of FOSL2 significantly inhibited NASH-associated hepatocyte pyroptosis, which was significantly reversed after overexpression of LY6D. Moreover, the promotion of hepatocyte pyroptosis by the FOSL2/LY6D axis was significantly attenuated by specific inhibition of NLRP3. These findings suggesting that FOSL2/LY6D axis may be a key molecular axis and a potential target for NASH therapeutics.","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 6","pages":"1752-1765"},"PeriodicalIF":4.3,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40584186","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: 2

Astragaloside IV alleviates senescence of vascular smooth muscle cells through activating Parkin-mediated mitophagy. 黄芪甲苷通过激活帕金森介导的有丝分裂来缓解血管平滑肌细胞的衰老。

IF 4.3 3区生物学

Human Cell Pub Date : 2022-11-01 Epub Date: 2022-08-04 DOI: 10.1007/s13577-022-00758-6

Huijun Li, Jialin Xu, Yanan Zhang, Lei Hong, Zhijian He, Zhiheng Zeng, Li Zhang

{"title":"Astragaloside IV alleviates senescence of vascular smooth muscle cells through activating Parkin-mediated mitophagy.","authors":"Huijun Li, Jialin Xu, Yanan Zhang, Lei Hong, Zhijian He, Zhiheng Zeng, Li Zhang","doi":"10.1007/s13577-022-00758-6","DOIUrl":"https://doi.org/10.1007/s13577-022-00758-6","url":null,"abstract":"Astragaloside IV (AS-IV), as one of the main active components of Astragalus membranaceus, has been reported to have cardiovascular protective effects. However, the role and molecular mechanism of AS-IV in vascular senescence have not been clearly stated. The in vitro aging model was constructed using bleomycin (BLM) in vascular smooth muscle cells (VSMCs). Cell senescence were assessed through Western blotting analysis of aging markers, flow cytometry, and the β-galactosidase (SA-β-Gal) kit. Mitophagy was determined through transmission electron microscopy, TMRM staining, and Western blotting analysis of p62. A model of aging blood vessels was induced by D-gal. The vascular wall thickness of mice was also evaluated by H&E staining. Our data proved that AS-IV plays an anti-senescent role in vitro and in vivo. Results showed that AS-IV effectively improved mitochondrial injury, raised MMP, and mediated mitophagy in BLM-induced senescent VSMCs and D-gal induced aging mice. Parkin expression strengthened AS-IV's anti-senescent function. In conclusions, AS-IV attenuated BLM-induced VSMC senescence via Parkin to regulate mitophagy. Therefore, AS-IV-mediated Parkin might be a latent therapeutic agent and target for VSMC senescence.","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 6","pages":"1684-1696"},"PeriodicalIF":4.3,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9515037/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40691571","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: 5

MicroRNA-149-3p expression correlates with outcomes of adrenocortical tumor patients and affects proliferation and cell cycle progression of H295A adrenocortical cancer cell line. MicroRNA-149-3p的表达与肾上腺皮质肿瘤患者的预后相关，影响H295A肾上腺皮质癌细胞系的增殖和细胞周期进展。

IF 4.3 3区生物学

Human Cell Pub Date : 2022-11-01 Epub Date: 2022-09-02 DOI: 10.1007/s13577-022-00778-2

Keteryne Rodrigues da Silva, Luciana Chain Veronez, Carolina Alves Pereira Correa, Régia Caroline Peixoto Lira, Mirella Baroni, Rosane de Paula Silva Queiroz, Sonir Roberto Rauber Antonini, José Andres Yunes, Silvia Regina Brandalise, Luiz Gonzaga Tone, Carlos Alberto Scrideli

{"title":"MicroRNA-149-3p expression correlates with outcomes of adrenocortical tumor patients and affects proliferation and cell cycle progression of H295A adrenocortical cancer cell line.","authors":"Keteryne Rodrigues da Silva, Luciana Chain Veronez, Carolina Alves Pereira Correa, Régia Caroline Peixoto Lira, Mirella Baroni, Rosane de Paula Silva Queiroz, Sonir Roberto Rauber Antonini, José Andres Yunes, Silvia Regina Brandalise, Luiz Gonzaga Tone, Carlos Alberto Scrideli","doi":"10.1007/s13577-022-00778-2","DOIUrl":"https://doi.org/10.1007/s13577-022-00778-2","url":null,"abstract":"Pediatric adrenocortical tumor (ACT) is a rare and aggressive neoplasm, with incidence in southern and southeastern Brazil 10-15 times higher than worldwide. Although microRNAs (miRNAs) have been reported to act as tumor suppressors or oncogenes in several cancers, the role of miR-149-3p in ACT remains unknown. In this study, we evaluated the expression of miR-149-3p in 67 pediatric ACT samples and 19 non-neoplastic adrenal tissues. The overexpression of miR-149-3p was induced in H295A cell line, and cell viability, proliferation, colony formation, and cell cycle were assessed by in miR-149-3p mimic or mimic control. In silico analysis were used to predict miR-149-3p putative target genes. CDKN1A expression at the mRNA and protein levels was evaluated by qRT-PCR and western blot, respectively. Higher miR-149-3p expression was associated with unfavorable ACT outcomes. Compared to the mimic control, miR-149-3p overexpression increased cell viability and colony formation, and affected cell cycle progression. Also, we identified CDKN1A as a potential miR-149-3p target gene, with decreased expression at both the gene and protein levels in miR-149-3p mimic cells. Collectively, these findings suggest that miR-149-3p promotes H295A cell viability by downregulating CDKN1A and provide evidence that miR-149-3p may be useful as a novel therapeutic target for pediatric ACT.","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 6","pages":"1952-1960"},"PeriodicalIF":4.3,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40343913","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: 2