Journal of Cellular and Molecular Medicine最新文献

Downregulation of p300/CBP-associated factor inhibits cardiomyocyte apoptosis via suppression of NF-κB pathway in ischaemia/reperfusion injury rats. 下调p300/ cbp相关因子通过抑制NF-κB通路抑制缺血再灌注损伤大鼠心肌细胞凋亡。

IF 5.3 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2021-10-01 DOI: 10.17632/B85NVYGP5F.1

Liqiang Qiu

{"title":"Downregulation of p300/CBP-associated factor inhibits cardiomyocyte apoptosis via suppression of NF-κB pathway in ischaemia/reperfusion injury rats.","authors":"Liqiang Qiu","doi":"10.17632/B85NVYGP5F.1","DOIUrl":"https://doi.org/10.17632/B85NVYGP5F.1","url":null,"abstract":"Cardiomyocyte apoptosis is the main reason of cardiac injury after myocardial ischaemia-reperfusion (I/R) injury (MIRI), but the role of p300/CBP-associated factor (PCAF) on myocardial apoptosis in MIRI is unknown. The aim of this study was to investigate the main mechanism of PCAF modulating cardiomyocyte apoptosis in MIRI. The MIRI model was constructed by ligation of the rat left anterior descending coronary vessel for 30 min and reperfusion for 24 h in vivo. H9c2 cells were harvested after induced by hypoxia for 6 h and then reoxygenation for 24 h (H/R) in vitro. The RNA interference PCAF expression adenovirus was transfected into rat myocardium and H9c2 cells. The area of myocardial infarction, cardiac function, myocardial injury marker levels, apoptosis, inflammation and oxidative stress were detected respectively. Both I/R and H/R remarkably upregulated the expression of PCAF, and downregulation of PCAF significantly attenuated myocardial apoptosis, inflammation and oxidative stress caused by I/R and H/R. In addition, downregulation of PCAF inhibited the activation of NF-κB signalling pathway in cardiomyocytes undergoing H/R. Pretreatment of lipopolysaccharide, a NF-κB pathway activator, could blunt these protective effects of PCAF downregulation on myocardial apoptosis in MIRI. These results highlight that downregulation of PCAF could reduce cardiomyocyte apoptosis by inhibiting the NF-κB pathway, thereby providing protection for MIRI. Therefore, PCAF might be a promising target for protecting against cardiac dysfunction induced by MIRI.","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78654082","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Korean Domestic Trends of Clinical Research and Direction of Intervention for Fibromyalgia 国内纤维肌痛的临床研究趋势及干预方向

IF 5.3 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2020-12-30 DOI: 10.30581/JCMM.2020.15.2.43

Lee Jung-han, Ji-Hye Geum, Hyeonjun Woo, C. Lee, C. Chung, Myeung-Su Lee

引用次数: 0

Application of Joint Mobilizing Chuna Following Tibial Plateau Fracture Surgery: A Study of Two Cases 胫骨平台骨折手术后关节动员法的应用:两例研究

IF 5.3 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2020-12-30 DOI: 10.30581/JCMM.2020.15.2.75

Eunbyul Cho, N. Cho

引用次数: 1

Identification of novel susceptibility loci for non-syndromic cleft lip with or without cleft palate. 非综合征性唇裂伴或不伴腭裂的新易感位点的鉴定。

IF 5.3 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2020-12-01 Epub Date: 2020-10-27 DOI: 10.1111/jcmm.15878

Lan Ma, Shu Lou, Ziyue Miao, Siyue Yao, Xin Yu, Shiyi Kan, Guirong Zhu, Fan Yang, Chi Zhang, Weibing Zhang, Meilin Wang, Lin Wang, Yongchu Pan

{"title":"Identification of novel susceptibility loci for non-syndromic cleft lip with or without cleft palate.","authors":"Lan Ma, Shu Lou, Ziyue Miao, Siyue Yao, Xin Yu, Shiyi Kan, Guirong Zhu, Fan Yang, Chi Zhang, Weibing Zhang, Meilin Wang, Lin Wang, Yongchu Pan","doi":"10.1111/jcmm.15878","DOIUrl":"https://doi.org/10.1111/jcmm.15878","url":null,"abstract":"Although several genome-wide association studies (GWAS) of non-syndromic cleft lip with or without cleft palate (NSCL/P) have been reported, more novel association signals are remained to be exploited. Here, we performed an in-depth analysis of our previously published Chinese GWAS cohort study with replication in an extra dbGaP case-parent trios and another in-house Nanjing cohort, and finally identified five novel significant association signals (rs11119445: 3' of SERTAD4, P = 6.44 × 10-14 ; rs227227 and rs12561877: intron of SYT14, P = 5.02 × 10-13 and 2.80 × 10-11 , respectively; rs643118: intron of TRAF3IP3, P = 4.45 × 10-6 ; rs2095293: intron of NR6A1, P = 2.98 × 10-5 ). The mean (standard deviation) of the weighted genetic risk score (wGRS) from these SNPs was 1.83 (0.65) for NSCL/P cases and 1.58 (0.68) for controls, respectively (P = 2.67 × 10-16 ). Rs643118 was identified as a shared susceptible factor of NSCL/P among Asians and Europeans, while rs227227 may contribute to the risk of NSCL/P as well as NSCPO. In addition, sertad4 knockdown zebrafish models resulted in down-regulation of sox2 and caused oedema around the heart and mandibular deficiency, compared with control embryos. Taken together, this study has improved our understanding of the genetic susceptibility to NSCL/P and provided further clues to its aetiology in the Chinese population.","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/jcmm.15878","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38628229","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: 4

Loganetin and 5-fluorouracil synergistically inhibit the carcinogenesis of gastric cancer cells via down-regulation of the Wnt/β-catenin pathway. 马尾草素与5-氟尿嘧啶通过下调Wnt/β-catenin通路协同抑制胃癌细胞的癌变。

IF 5.3 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2020-12-01 Epub Date: 2020-10-24 DOI: 10.1111/jcmm.15932

Huaixiang Zhou, Xiaoge Hu, Na Li, Guangyan Li, Xiaotian Sun, Feimin Ge, Jiahong Jiang, Jingchun Yao, Dongsheng Huang, Liu Yang

{"title":"Loganetin and 5-fluorouracil synergistically inhibit the carcinogenesis of gastric cancer cells via down-regulation of the Wnt/β-catenin pathway.","authors":"Huaixiang Zhou, Xiaoge Hu, Na Li, Guangyan Li, Xiaotian Sun, Feimin Ge, Jiahong Jiang, Jingchun Yao, Dongsheng Huang, Liu Yang","doi":"10.1111/jcmm.15932","DOIUrl":"https://doi.org/10.1111/jcmm.15932","url":null,"abstract":"Although most gastrointestinal tumours are sensitive to 5-fluorouracil (5FU), drug resistance is commonly occurred after 5FU therapy in gastric cancer (GC). Loganetin is the primary active compound in Cornus officinali. However, the synergetic effects of loganetin and 5FU on GC remain unknown. Here, we investigated the synergetic effects and the underlying mechanism of loganetin and 5FU on proliferation, stem-like properties, migration, and invasion of GC both in vitro and in vivo. We found that loganetin alone inhibited the proliferation, stem-like properties, migration and invasion of GC cells in vitro. Importantly, the loganetin remarkably enhanced the anti-cancer effect of 5FU on GC cells and the Wnt/β-catenin pathway might be involved in this process. Animal experiments further confirmed the synergistic effects of 5FU and loganetin on inhibiting cell growth and metastasis of GC. These results suggested that loganetin could synergistically increase the effect of 5FU against GC, which sheds light on effective combinational drug strategies for GC treatment.","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/jcmm.15932","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38524850","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

Neurotrophin-3 stimulates stem Leydig cell proliferation during regeneration in rats. 神经营养因子-3刺激大鼠干细胞再生过程中的间质细胞增殖。

IF 5.3 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2020-12-01 Epub Date: 2020-10-22 DOI: 10.1111/jcmm.15886

Yige Yu, Zengqiang Li, Feifei Ma, Quanxu Chen, Liben Lin, Qiang Xu, Yang Li, Xiu Xin, Peipei Pan, Tongliang Huang, Yiyan Wang, Qianjin Fei, Ren-Shan Ge

{"title":"Neurotrophin-3 stimulates stem Leydig cell proliferation during regeneration in rats.","authors":"Yige Yu, Zengqiang Li, Feifei Ma, Quanxu Chen, Liben Lin, Qiang Xu, Yang Li, Xiu Xin, Peipei Pan, Tongliang Huang, Yiyan Wang, Qianjin Fei, Ren-Shan Ge","doi":"10.1111/jcmm.15886","DOIUrl":"https://doi.org/10.1111/jcmm.15886","url":null,"abstract":"Neurotrophin-3 (NT-3) acts as an important growth factor to stimulate and control tissue development. The NT-3 receptor, TRKC, is expressed in rat testis. Its function in regulation of stem Leydig cell development and its underlying mechanism remain unknown. Here, we reported the role of NT-3 to regulate stem Leydig cell development in vivo and in vitro. Ethane dimethane sulphonate was used to kill all Leydig cells in adult testis, and NT-3 (10 and 100 ng/testis) was injected intratesticularly from the 14th day after ethane dimethane sulphonate injection for 14 days. NT-3 significantly reduced serum testosterone levels at doses of 10 and 100 ng/testis without affecting serum luteinizing hormone and follicle-stimulating hormone levels. NT-3 increased CYP11A1-positive Leydig cell number at 100 ng/testis and lowered Leydig cell size and cytoplasmic size at doses of 10 and 100 ng/testis. After adjustment by the Leydig cell number, NT-3 significantly down-regulated the expression of Leydig cell genes (Lhcgr, Scarb1, Star, Cyp11a1, Hsd3b1, Cyp17a1, Hsd17b3, Hsd11b1, Insl3, Trkc and Nr5a1) and the proteins. NT-3 increased the phosphorylation of AKT1 and mTOR, decreased the phosphorylation of 4EBP, thereby increasing ATP5O. In vitro study showed that NT-3 dose-dependently stimulated EdU incorporation into stem Leydig cells and inhibited stem Leydig cell differentiation into Leydig cells, thus leading to lower medium testosterone levels and lower expression of Lhcgr, Scarb1, Trkc and Nr5a1 and their protein levels. NT-3 antagonist Celitinib can antagonize NT-3 action in vitro. In conclusion, the present study demonstrates that NT-3 stimulates stem Leydig cell proliferation but blocks the differentiation via TRKC receptor.","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/jcmm.15886","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38620890","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: 6

Anti-inflammatory and immune-modulatory impacts of berberine on activation of autoreactive T cells in autoimmune inflammation. 小檗碱对自身免疫性炎症中自身反应性T细胞活化的抗炎和免疫调节作用。

IF 5.3 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2020-12-01 Epub Date: 2020-11-01 DOI: 10.1111/jcmm.16049

Seyed-Morteza Ehteshamfar, Masoume Akhbari, Jalil Tavakol Afshari, Motahareh Seyedi, Banafsheh Nikfar, Abbas Shapouri-Moghaddam, Erfan Ghanbarzadeh, Amir Abbas Momtazi-Borojeni

{"title":"Anti-inflammatory and immune-modulatory impacts of berberine on activation of autoreactive T cells in autoimmune inflammation.","authors":"Seyed-Morteza Ehteshamfar, Masoume Akhbari, Jalil Tavakol Afshari, Motahareh Seyedi, Banafsheh Nikfar, Abbas Shapouri-Moghaddam, Erfan Ghanbarzadeh, Amir Abbas Momtazi-Borojeni","doi":"10.1111/jcmm.16049","DOIUrl":"10.1111/jcmm.16049","url":null,"abstract":"Autoreactive inflammatory CD4+ T cells, such as T helper (Th)1 and Th17 subtypes, have been found to associate with the pathogenesis of autoimmune disorders. On the other hand, CD4+ Foxp3+ T regulatory (Treg) cells are crucial for the immune tolerance and have a critical role in the suppression of the excessive immune and inflammatory response promoted by these Th cells. In contrast, dendritic cells (DCs) and macrophages are immune cells that through their inflammatory functions promote autoreactive T-cell responses in autoimmune conditions. In recent years, there has been increasing attention to exploring effective immunomodulatory or anti-inflammatory agents from the herbal collection of traditional medicine. Berberine, an isoquinoline alkaloid, is one of the main active ingredients extracted from medicinal herbs and has been shown to exert various biological and pharmacological effects that are suggested to be mainly attributed to its anti-inflammatory and immunomodulatory properties. Several lines of experimental study have recently investigated the therapeutic potential of berberine for treating autoimmune conditions in animal models of human autoimmune diseases. Here, we aimed to seek mechanisms underlying immunomodulatory and anti-inflammatory effects of berberine on autoreactive inflammatory responses in autoimmune conditions. Reported data reveal that berberine can directly suppress functions and differentiation of pro-inflammatory Th1 and Th17 cells, and indirectly decrease Th cell-mediated inflammation through modulating or suppressing other cells assisting autoreactive inflammation, such as Tregs, DCs and macrophages.","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/jcmm.16049","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38659459","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: 48

Disruption of microRNA-214 during general anaesthesia prevents brain injury and maintains mitochondrial fusion by promoting Mfn2 interaction with Pkm2. 在全身麻醉期间，microRNA-214的破坏可防止脑损伤，并通过促进Mfn2与Pkm2的相互作用来维持线粒体融合。

IF 5.3 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2020-12-01 Epub Date: 2020-11-04 DOI: 10.1111/jcmm.15222

Tiejun Liu, Bin Wang, Gai Li, Xiaoliu Dong, Guannan Yu, Qingzeng Qian, Likun Duan, Hongxia Li, Zhao Jia, Jing Bai

{"title":"Disruption of microRNA-214 during general anaesthesia prevents brain injury and maintains mitochondrial fusion by promoting Mfn2 interaction with Pkm2.","authors":"Tiejun Liu, Bin Wang, Gai Li, Xiaoliu Dong, Guannan Yu, Qingzeng Qian, Likun Duan, Hongxia Li, Zhao Jia, Jing Bai","doi":"10.1111/jcmm.15222","DOIUrl":"10.1111/jcmm.15222","url":null,"abstract":"Duration of surgical general anaesthesia is associated with severe brain injury and neurological deficits. The specific mechanisms underlying post-general anaesthesia brain injury, however, still remain to be elucidated. Herein, we explore the role of microRNA-214 (miR-214) in the occurrence of brain injury after general anaesthesia and its underlying mechanism. Hippocampal tissues and neurons were isolated from rats exposed to 2% sevoflurane. TUNEL stains reflect hippocampal neuron apoptosis. Cultured hippocampal neurons stained with JC-1 and MitoTracker dyes were imaged by fluorescence microscope to visualize changes of mitochondrial membrane potential and mitochondrial fusion. Mitochondrial function was evaluated. Mitofusin 2 (Mfn2) binding to miR-214 or pyruvate kinase M2 (Pkm2) was confirmed by co-immunoprecipitation, immunofluorescence, dual luciferase reporter gene and RNA immunoprecipitation assays. After exposure to 2% sevoflurane, up-regulated miR-214 expression and impaired interaction between Mfn2 and Pkm2 were found in rat hippocampal tissues. Rats exposed to 2% sevoflurane also experienced neuronal injury, mitochondrial defects and deficits in the brain-derived neurotrophic factor (Bdnf) signalling. miR-214 was shown to target Mfn2 by impairing its binding with Pkm2. Inhibiting miR-214 expression using its specific inhibitor improved mitochondrial membrane potential, enhanced mitochondrial fusion, maintained mitochondrial function, restored interaction between Mfn2 and Pkm2, and activated the Bdnf signalling in cultured hippocampal neurons. Adenovirus infection of miR-214 inhibitor reduced neuron apoptosis and maintained mitochondrial function in the hippocampus of rats exposed to 2% sevoflurane. Taken together, the study demonstrates inhibition of miR-214 is cerebral protective against brain injury following general anaesthesia.","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/jcmm.15222","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38567377","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: 7

Methylprednisolone alleviates multiple sclerosis by expanding myeloid-derived suppressor cells via glucocorticoid receptor β and S100A8/9 up-regulation. 甲基强的松龙通过糖皮质激素受体β和S100A8/9上调，扩大髓源性抑制细胞，从而缓解多发性硬化。

IF 5.3 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2020-12-01 Epub Date: 2020-10-23 DOI: 10.1111/jcmm.15928

Zhongkun Wang, Ge Zheng, Guangjian Li, Mengkun Wang, Zhanchuan Ma, Huimin Li, Xiang-Yang Wang, Huanfa Yi

{"title":"Methylprednisolone alleviates multiple sclerosis by expanding myeloid-derived suppressor cells via glucocorticoid receptor β and S100A8/9 up-regulation.","authors":"Zhongkun Wang, Ge Zheng, Guangjian Li, Mengkun Wang, Zhanchuan Ma, Huimin Li, Xiang-Yang Wang, Huanfa Yi","doi":"10.1111/jcmm.15928","DOIUrl":"https://doi.org/10.1111/jcmm.15928","url":null,"abstract":"Methylprednisolone is an effective drug in the treatment of autoimmune disease, such as multiple sclerosis (MS), due to long-acting anti-inflammatory, antiallergic and immunosuppressant. Previous studies have noted the importance of myeloid-derived suppressor cells (MDSC) in MS progression. However, it is still not known whether methylprednisolone could influence the ratio and function of MDSC during MS treatment. In the current study, we found an increased ratio of MDSC at the onset of EAE in mice model; but methylprednisolone pulse therapy (MPPT) did not alter the percentage and suppressive function of MDSC during disease attenuation. However, the percentage of G-MDSC in PBMC significantly increased in patients with MS. Surprisingly, relapsing MS patients showed a significant increase in both M-MDSC and G-MDSC after MPPT. The disease remission positively correlated expansion of MDSC and expression of arginase-1. Additionally, MPPT reduced the expression of inhibitory glucocorticoid (GCs) receptor β subunit on MDSC while elevating serum levels of immune regulatory S100A8/A9 heterodimer. Thus, MDSC dynamics and function in mouse EAE differ from those in human MS during MPPT. Our study suggested that GCs treatment may help relieve the acute phase of MS by expanding MDSC through up-regulating of GR signalling and S100A8/A9 heterodimers.","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/jcmm.15928","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38521847","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: 14

IFN-γ⁺ IL-17⁺ Th17 cells regulate fibrosis through secreting IL-21 in systemic scleroderma. IFN-γ+ IL-17+ Th17细胞通过分泌IL-21调节系统性硬皮病纤维化。

IF 5.3 2区医学

Journal of Cellular and Molecular Medicine Pub Date : 2020-12-01 Epub Date: 2020-11-06 DOI: 10.1111/jcmm.15266

Xiaojing Xing, Anqi Li, Hong Tan, Yong Zhou

{"title":"IFN-γ+ IL-17+ Th17 cells regulate fibrosis through secreting IL-21 in systemic scleroderma.","authors":"Xiaojing Xing, Anqi Li, Hong Tan, Yong Zhou","doi":"10.1111/jcmm.15266","DOIUrl":"https://doi.org/10.1111/jcmm.15266","url":null,"abstract":"This study aimed to explore the function of IFN-γ+ IL-17+ Th17 cells on fibrosis in systemic scleroderma (SSc). Blood and skin samples were collected from 20 SSc cases and 10 healthy individuals. The percentage of IFN-γ+ IL-17+ Th17 cells was detected using flow cytometry. The in vitro induction of IFN-γ+ IL-17+ Th17 cells was performed adopting PHA and rIL-12. Gene expression was detected via quantitative real-time polymerase chain reaction (qRT-PCR), whereas western blot analysis was adopted for protein analysis. The distribution of IFN-γ+ IL-17+ Th17 cells was significantly increased in SSc cases and positively correlated with SSc stages (P = .031), disease duration (P = .016), activity (P = .025) and skin scores (P < .001). In vitro, IFN-γ+ IL-17+ Th17 cells could promote the expressions of α-SMA and COL1A1, revealing increased fibroblasts' proliferation and enhanced collagen-secreting capacity. In addition, IL-21 expression was significantly increased in co-culture medium of IFN-γ+ IL-17+ Th17 cells and fibroblasts (P < .001). IL-21 neutralizer treatment resulted in the down-regulation of α-SMA and COL1A1. IL-21 was confirmed as an effector of IFN-γ+ IL-17+ Th17 cells in fibrosis process. The distribution of IFN-γ+ IL-17+ Th17 cells was significantly increased in SSc cases and positively correlated with disease activity. IFN-γ+ IL-17+ Th17 cells could promote fibroblast proliferation and enhance collagen-secreting ability via producing IL-21, thus contributing to fibrosis in SSc.","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/jcmm.15266","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38574944","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: 20