Journal of Cellular and Molecular Medicine最新文献_第4页

Maackiain dampens osteoclastogenesis via attenuating RANKL-stimulated NF-κB signalling pathway and NFATc1 activity. Maackiain通过减弱rankl刺激的NF-κB信号通路和NFATc1活性来抑制破骨细胞的发生。

IF 5.3 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2020-11-01 Epub Date: 2020-09-16 DOI: 10.1111/jcmm.15647

Yuhao Liu, Weizai Zeng, Chao Ma, Ziyi Wang, Chao Wang, Shaobin Li, Wei He, Qingwen Zhang, Jiake Xu, Chi Zhou

{"title":"Maackiain dampens osteoclastogenesis via attenuating RANKL-stimulated NF-κB signalling pathway and NFATc1 activity.","authors":"Yuhao Liu, Weizai Zeng, Chao Ma, Ziyi Wang, Chao Wang, Shaobin Li, Wei He, Qingwen Zhang, Jiake Xu, Chi Zhou","doi":"10.1111/jcmm.15647","DOIUrl":"https://doi.org/10.1111/jcmm.15647","url":null,"abstract":"Osteolytic diseases are typified by over-enhanced formation and resorbing function of osteoclasts and have a major impact on human health. Inhibition of osteoclastic differentiation and function is a key strategy for clinical therapy of osteolytic conditions. Maackiain is a natural compound extracted from Sophora flavescens, which has been applied to anti-allergic and anti-tumour treatments. The present results showed that Maackiain could restrain receptor activator of nuclear factor-κB ligand (RANKL)-stimulated osteoclast formation and hydroxyapatite resorption dose-dependently, and interrupt the structures of F-actin belts in the mature osteoclasts. It also repressed the expressions of osteoclast-specific genes and proteins. Furthermore, Maackiain could inhibit RANKL-stimulated NF-κB and calcium signalling pathways, and dampen Nuclear factor of activated T cell cytoplasmic 1 activity, protein expression and translocation into the nucleus. These results revealed that Maackiain may have a potential therapeutic effect on osteoclast-related disorders.","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2020-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/jcmm.15647","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38388322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 12

Effect of rs4719839 polymorphism on risk of ventilator-associated pneumonia, expression of microRNA-148 and autophagy-related 16-like 1 (ATG16L1). rs4719839多态性对呼吸机相关性肺炎风险、microRNA-148表达和自噬相关16样1 (ATG16L1)的影响

IF 5.3 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2020-11-01 Epub Date: 2020-09-17 DOI: 10.1111/jcmm.15824

Shu-Peng Wang, Wen Li, Chen Li, Xue-Yan Duan, Jun Duan

{"title":"Effect of rs4719839 polymorphism on risk of ventilator-associated pneumonia, expression of microRNA-148 and autophagy-related 16-like 1 (ATG16L1).","authors":"Shu-Peng Wang, Wen Li, Chen Li, Xue-Yan Duan, Jun Duan","doi":"10.1111/jcmm.15824","DOIUrl":"https://doi.org/10.1111/jcmm.15824","url":null,"abstract":"MiR-148 is a negative regulator of autophagy 16-like 1 (ATG16L1), a gene implicated in the pathogenesis of ventilator-associated pneumonia (VAP). Therefore, the role of miR-148 polymorphism in the pathogenesis of VAP was studied here. The expression of miR-148, ATG16L1, Beclin-I, LC3-II, TNF-α and IL-6 in serum and peripheral blood mononuclear cells (PBMCs) of VAP patients was detected to study their relationship in the pathogenesis of VAP. Chronic obstructive pulmonary disease patients carrying the AA/AG genotypes of miR-148 rs4719839 single nucleotide polymorphism (SNP) were more prone to VAP due to the higher expression of miR-148, TNF-α and IL-6 along with suppressed expression of ATG16L1, Beclin-I and LC3-II in their serum and PBMCs. Transfection of miR-148 mimics to primary PBMCs genotyped as GG and AA decreased the expression of ATG16L1, Beclin-I and LC3-II. Finally, cells carrying the AA genotype of rs4719839 SNP were more sensitive to the role of LPS stimulation in suppressing ATG16L1, Beclin-I and LC3-II expression while activating TNF-α and IL-6 expression. Our work presented detailed evidence, suggesting that the rs4719839 polymorphism can affect the risk of VAP.","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2020-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/jcmm.15824","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38390933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 5

C-Cbl regulates c-MPL receptor trafficking and its internalization. C-Cbl调节c-MPL受体的转运及其内化。

IF 5.3 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2020-11-01 Epub Date: 2020-09-20 DOI: 10.1111/jcmm.15785

Melanie Märklin, Claudia Tandler, Hans-Georg Kopp, Kyle L Hoehn, Leticia Quintanilla-Martinez, Oliver Borst, Martin R Müller, Sebastian J Saur

引用次数: 5

Long non-coding RNA MEG3 inhibits M2 macrophage polarization by activating TRAF6 via microRNA-223 down-regulation in viral myocarditis. 长链非编码RNA MEG3在病毒性心肌炎中通过microRNA-223下调激活TRAF6抑制M2巨噬细胞极化。

IF 5.3 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2020-11-01 Epub Date: 2020-10-13 DOI: 10.1111/jcmm.15720

Yu-Long Xue, Sheng-Xiao Zhang, Chao-Feng Zheng, Yu-Feng Li, Li-Hui Zhang, Qin-Yi Su, Yu-Fei Hao, Shu Wang, Xue-Wen Li

{"title":"Long non-coding RNA MEG3 inhibits M2 macrophage polarization by activating TRAF6 via microRNA-223 down-regulation in viral myocarditis.","authors":"Yu-Long Xue, Sheng-Xiao Zhang, Chao-Feng Zheng, Yu-Feng Li, Li-Hui Zhang, Qin-Yi Su, Yu-Fei Hao, Shu Wang, Xue-Wen Li","doi":"10.1111/jcmm.15720","DOIUrl":"https://doi.org/10.1111/jcmm.15720","url":null,"abstract":"Viral myocarditis (VMC) commonly triggers heart failure, for which no specific treatments are available. This study aims to explore the specific role of long non-coding RNA (lncRNA) maternally expressed 3 (MEG3) in VMC. A VMC mouse model was induced by Coxsackievirus B3 (CVB3). Then, MEG3 and TNF receptor-associated factor 6 (TRAF6) were silenced and microRNA-223 (miR-223) was over-expressed in the VMC mice, followed by determination of ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS). Dual-luciferase reporter assay was introduced to test the interaction among MEG3, TRAF6 and miR-223. Macrophages were isolated from cardiac tissues and bone marrow, and polarization of M1 or M2 macrophages was induced. Then, the expressions of components of NLRP3 inflammatory body (NLRP3, ASC, Caspase-1), M1 markers (CD86, iNOS and TNF-α) and M2 markers (CD206, Arginase-1 and Fizz-1) were measured following MEG3 silencing. In the VMC mouse model, MEG3 and TRAF6 levels were obviously increased, while miR-223 expression was significantly reduced. Down-regulation of MEG3 resulted in the inhibition of TRAF6 by promoting miR-223. TRAF6 was negatively correlated with miR-223, but positively correlated with MEG3 expression. Down-regulations of MEG3 or TRAF6 or up-regulation of miR-223 was observed to increase mouse weight, survival rate, LVEF and LVFS, while inhibiting myocarditis and inflammation via the NF-κB pathway inactivation in VMC mice. Down-regulation of MEG3 decreased M1 macrophage polarization and elevated M2 macrophage polarization by up-regulating miR-223. Collectively, down-regulation of MEG3 leads to the inhibition of inflammation and induces M2 macrophage polarization via miR-223/TRAF6/NF-κB axis, thus alleviating VMC.","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2020-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/jcmm.15720","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38480419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 36

Respiratory syncytial virus infection-induced mucus secretion by down-regulation of miR-34b/c-5p expression in airway epithelial cells. 呼吸道合胞病毒感染通过下调气道上皮细胞miR-34b/c-5p表达诱导粘液分泌。

IF 5.3 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2020-11-01 Epub Date: 2020-09-16 DOI: 10.1111/jcmm.15845

Xizi Du, Yu Yang, Gelei Xiao, Ming Yang, Lin Yuan, Ling Qin, Ruoxi He, Leyuan Wang, Mengping Wu, ShuangYan Wu, Juntao Feng, Yang Xiang, Xiangping Qu, Huijun Liu, Xiaoqun Qin, Chi Liu

{"title":"Respiratory syncytial virus infection-induced mucus secretion by down-regulation of miR-34b/c-5p expression in airway epithelial cells.","authors":"Xizi Du, Yu Yang, Gelei Xiao, Ming Yang, Lin Yuan, Ling Qin, Ruoxi He, Leyuan Wang, Mengping Wu, ShuangYan Wu, Juntao Feng, Yang Xiang, Xiangping Qu, Huijun Liu, Xiaoqun Qin, Chi Liu","doi":"10.1111/jcmm.15845","DOIUrl":"https://doi.org/10.1111/jcmm.15845","url":null,"abstract":"Severe RSV infection is the main cause of hospitalization to children under the age of five. The regulation of miRNAs on the severity of RSV infection is unclear. The aim of the study was to identify the critical differential expression miRNAs (DE miRNAs) that can regulate the pathological response in RSV-infected airway epithelial cells. In this study, miRNA and mRNA chips of RSV-infected airway epithelia from Gene Expression Omnibus (GEO) were screened and analysed, separately. DE miRNAs-targeted genes were performed for further pathway and process enrichment analysis. DE miRNA-targeted gene functional network was constructed on the basis of miRNA-mRNA interaction. The screened critical miRNA was also investigated by bioinformatics analysis. Then, RSV-infected human bronchial epithelial cells (HBECs) were constructed to verify the expression of the DE miRNAs. Finally, specific synthetic DE miRNAs mimics were used to confirm the effect of DE miRNAs on the RSV-infected HBECs. 45 DE miRNAs were identified from GEO62306 dataset. Our results showed that hsa-mir-34b-5p and hsa-mir-34c-5p decreased significantly in HBECs after RSV infection. Consistent with the biometric analysis, hsa-mir-34b/c-5p is involved in the regulation of mucin expression gene MUC5AC. In RSV-infected HBECs, the inducement of MUC5AC production by decreased hsa-mir-34b/c-5p was partly mediated through activation of c-Jun. These findings provide new insights into the mechanism of mucus obstruction after RSV infection and represent valuable targets for RSV infection and airway obstruction treatment.","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2020-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/jcmm.15845","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38485843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 16

Long non-coding RNA DLX6-AS1 mediates proliferation, invasion and apoptosis of endometrial cancer cells by recruiting p300/E2F1 in DLX6 promoter region. 长链非编码RNA DLX6- as1通过在DLX6启动子区募集p300/E2F1介导子宫内膜癌细胞的增殖、侵袭和凋亡。

IF 5.3 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2020-11-01 Epub Date: 2020-09-20 DOI: 10.1111/jcmm.15810

Hui Zhao, Qian Xu

{"title":"Long non-coding RNA DLX6-AS1 mediates proliferation, invasion and apoptosis of endometrial cancer cells by recruiting p300/E2F1 in DLX6 promoter region.","authors":"Hui Zhao, Qian Xu","doi":"10.1111/jcmm.15810","DOIUrl":"https://doi.org/10.1111/jcmm.15810","url":null,"abstract":"Endometrial cancer features abnormal growth of cells of the inner lining of the uterus with the potential to invade to other organs. Accumulating evidence suggests that aberrant expression of long non-coding RNA (lncRNA) may facilitate cancer progression. The aim of the present study was to identify the molecular mechanisms of the lncRNA known as DLX6 antisense RNA 1 (DLX6-AS1) in endometrial cancer. Microarray-based analysis was utilized to predict expression profile and possible function pattern of DLX6-AS1 and DLX6 in endometrial cancer, and their expression was quantified in 78 clinically obtained endometrial cancer tissues and also in cell lines. We next assessed the effects of DLX6-AS1 and DLX6 on proliferation, invasion and apoptosis of endometrial cancer cells. A mouse xenograft model was established to confirm DLX6-AS1 functions and explore its underlying regulatory mechanisms in vivo. DLX6-AS1 and DLX6 were highly expressed in endometrial cancer tissues and cells, and their silencing weakened the proliferative and invasive abilities of endometrial cancer cells and tumours, while promoting apoptosis. Mechanistic investigations indicated that DLX6-AS1 formed a triplex structure with DLX6 via interaction with p300/E2F1 acetyltransferase. Thus, we find that functional up-regulation of DLX6-AS1 can promote endometrial cancer progression via a novel triplex mechanism that may prove to be great clinical significance for future treatments of endometrial cancer.","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2020-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/jcmm.15810","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38498478","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 18

PLA2G16 is a mutant p53/KLF5 transcriptional target and promotes glycolysis of pancreatic cancer. PLA2G16是突变型p53/KLF5转录靶点，促进胰腺癌糖酵解。

IF 5.3 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2020-11-01 Epub Date: 2020-09-27 DOI: 10.1111/jcmm.15832

Wei Xia, Hansong Bai, Ying Deng, Yi Yang

{"title":"PLA2G16 is a mutant p53/KLF5 transcriptional target and promotes glycolysis of pancreatic cancer.","authors":"Wei Xia, Hansong Bai, Ying Deng, Yi Yang","doi":"10.1111/jcmm.15832","DOIUrl":"https://doi.org/10.1111/jcmm.15832","url":null,"abstract":"PLA2G16 is a member of the phospholipase family that catalyses the generation of lysophosphatidic acids (LPAs) and free fatty acids (FFAs) from phosphatidic acid. In the current study, we explored the functional role of PLA2G16 in pancreatic adenocarcinoma (PAAD) and the genetic/epigenetic alterations leading to its dysregulation. Bioinformatic analysis was performed using data from The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx) and the Human Protein Atlas (HPA). Then, PANC-1 and MIA-PaCa-2 cells harbouring TP53 mutations were used for cellular and animal studies. Results showed that PL2G16 expression was significantly up-regulated in PAAD tissue and was associated with unfavourable survival. PLA2G16 inhibition suppressed pancreatic cell growth in vitro and in vivo and also inhibited aerobic glycolysis. Bioinformatic analysis indicated that KLF5 was positively correlated with PLA2G16 expression in PAAD tumours with TP53 mutation. TP53 or KLF5 inhibition significantly reduced PLA2G16 expression at both mRNA and protein levels. Dual-luciferase and chromatin Immunoprecipitation-quantitative polymerase chain reaction assays showed that KLF5 directly bound to the PLA2G16 promoter and activated its transcription. Co-immunoprecipitation assay indicated that mutant p53 had a physical interaction with KLF5. Inhibition of mutant p53 impaired the transcriptional activating effects of KLF5. In PAAD cases in TCGA, PLA2G16 expression was positively correlated with its copy number (Pearson's r = 0.51, P < 0.001), but was strongly and negatively correlated with the methylation level of cg09518969 (Pearson's r = -0.64, P < 0.001), a 5'-cytosine-phosphodiester bond-guanine-3' site within its gene locus. In conclusion, this study revealed a novel mutant p53/KLF5-PLA2G16 regulatory axis on tumour growth and glycolysis in PAAD.","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2020-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/jcmm.15832","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38528113","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 13

Inhibitory effect of Ubenimex combined with fluorouracil on multiple drug resistance and P-glycoprotein expression level in non-small lung cancer. 乌苯尼美联合氟尿嘧啶对非小细胞肺癌多重耐药及p糖蛋白表达水平的抑制作用。

IF 5.3 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2020-11-01 Epub Date: 2020-09-17 DOI: 10.1111/jcmm.15875

Jun Wan, Xie-An Ling, Jian Wang, Guang-Gui Ding, Xi Wang

{"title":"Inhibitory effect of Ubenimex combined with fluorouracil on multiple drug resistance and P-glycoprotein expression level in non-small lung cancer.","authors":"Jun Wan, Xie-An Ling, Jian Wang, Guang-Gui Ding, Xi Wang","doi":"10.1111/jcmm.15875","DOIUrl":"https://doi.org/10.1111/jcmm.15875","url":null,"abstract":"Tumour drug resistance is one of the most urgent issues faced by anti-tumour therapies. P-glycoprotein (P-gp) has been reported to be correlated with drug resistance. In this study, we aimed to study the synergistic effect of fluorouracil (5FU) and Ubenimex (UBE) on drug resistance in lung cancer. In this study, the tumour inhibitory role of 5FU and UBE was assessed in nude mice bearing A549 or A549/ADR. Real-time polymerase chain reaction, Western blot and immunohistochemical were performed to analyse the mRNA and protein expression of P-gp. TUNEL assay was used to evaluate the apoptosis of A549/ADR cells under 5FU and UBE treatment. MTT assay was performed to calculate the IC50 value of 5FU and UBE in A549 or A549/ADR. Combined administration of 5FU and UBE significantly inhibited the tumour growth of multidrug-resistant cell lines A549/ADR in nude mice by down-regulating the mRNA and protein expression of P-gp. The apoptosis of A549/ADR was remarkably elevated in nude mice treated with 5FU and UBE. The IC50 value of 5FU and UBE was dramatically declined in A549/ADR cells compared with that of 5FU or UBE alone. Combined treatment of 5FU and UBE remarkably enhanced the apoptosis of A549/ADR cells by enhancing the intracellular accumulation of the drugs. The results of this study demonstrated that UBE combined with fluorouracil attenuated multiple drug resistance and inhibited the expression of P-gp in lung cancer.","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2020-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/jcmm.15875","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38392667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Naturally activated adaptive immunity in COVID-19 patients. COVID-19患者自然激活的适应性免疫

IF 5.3 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2020-11-01 Epub Date: 2020-09-25 DOI: 10.1111/jcmm.15771

Xiaofeng Yang, Tongxin Dai, Xiaobo Zhou, Hongbo Qian, Rui Guo, Lei Lei, Xingzhe Zhang, Dan Zhang, Lin Shi, Yanbin Cheng, Jinsong Hu, Yaling Guo, Baojun Zhang

{"title":"Naturally activated adaptive immunity in COVID-19 patients.","authors":"Xiaofeng Yang, Tongxin Dai, Xiaobo Zhou, Hongbo Qian, Rui Guo, Lei Lei, Xingzhe Zhang, Dan Zhang, Lin Shi, Yanbin Cheng, Jinsong Hu, Yaling Guo, Baojun Zhang","doi":"10.1111/jcmm.15771","DOIUrl":"https://doi.org/10.1111/jcmm.15771","url":null,"abstract":"Coronavirus disease-2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus (SARS-CoV-2) has rapidly spread worldwide, threatening the health and lives of many people. Unfortunately, information regarding the immunological characteristics of COVID-19 patients remains limited. Herein, we collected blood samples from 18 healthy donors (HDs) and 38 COVID-19 patients to analyse changes in the adaptive immune cell populations and their phenotypes. We observed that the lymphocyte percentage moderately decreased, CD4 and CD8 T cell percentage among lymphocytes were similar, and B cell percentage was increased in COVID-19 patients in comparison to that in HDs. T cells, especially CD8 T cells, showed an enhanced expression of late activation marker CD25 and exhaustion marker PD-1. Importantly, SARS-CoV-2 infection increased the percentage of T follicular helper- and germinal centre B-like cells in the blood. The parameters in COVID-19 patients remained unchanged across various age groups. Therefore, we demonstrated that the T and B cells are activated naturally and are functional during SARS-CoV-2 infection. These data provide evidence that the adaptive immunity in most patients could be primed to induce a significant immune response against SARS-CoV-2 infection upon receiving standard medical care.","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2020-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/jcmm.15771","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38419147","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 22

Knockdown of circ_0060745 alleviates acute myocardial infarction by suppressing NF-κB activation. 敲低circ_0060745可通过抑制NF-κB活化来缓解急性心肌梗死。

IF 5.3 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2020-11-01 Epub Date: 2020-09-25 DOI: 10.1111/jcmm.15748

Changlin Zhai, Gang Qian, Huajun Wu, Haihua Pan, Shuoyin Xie, Zhewei Sun, Pingyang Shao, Guanmin Tang, Huilin Hu, Song Zhang

{"title":"Knockdown of circ_0060745 alleviates acute myocardial infarction by suppressing NF-κB activation.","authors":"Changlin Zhai, Gang Qian, Huajun Wu, Haihua Pan, Shuoyin Xie, Zhewei Sun, Pingyang Shao, Guanmin Tang, Huilin Hu, Song Zhang","doi":"10.1111/jcmm.15748","DOIUrl":"https://doi.org/10.1111/jcmm.15748","url":null,"abstract":"It has been shown that circRNAs are involved in the development of heart diseases. However, few studies explored the role of circRNAs in acute myocardial infarction (AMI). The present study aims to investigate the role of circ_0060745 in the pathogenesis of AMI. We found that the expression of circ_0060745 was significantly increased in the myocardium of AMI mice and was mainly expressed in myocardial fibroblasts. The knockdown of circ_0060745 decreased myocardial infarct size and improved systolic cardiac functions after AMI. The knockdown of circ_0060745 in cardiac fibroblasts inhibited the migration of peritoneal macrophage, the apoptosis of cardiomyocytes and the expressions of IL-6, IL-12, IL-1β, TNF-α and NF-κB under hypoxia. Overexpression of circ_0060745 caused an increase in infarct size and worsened cardiac functions after AMI. In summary, our findings showed that knockdown of circ_0060745 mitigates AMI by suppressing cardiomyocyte apoptosis and inflammation. These protective effects could be attributed to inhibition of NF-κB activation.","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2020-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/jcmm.15748","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38420719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 21