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Search results for: NFATc3

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#33536917   2021/01/18 To Up

Tsantan Sumtang Restored Right Ventricular Function in Chronic Hypoxia-Induced Pulmonary Hypertension Rats.

Tsantan Sumtang originated from which consisted of (Roxb.) B. L. Burtt and A. W. Hill, L., and Houtt. The three herbs are in ratio 1:1:1. This medication is widely used for cardiovascular diseases. The purpose of this study was to explore the effect of Tsantan Sumtang on right ventricular (RV) function in hypoxia-induced pulmonary hypertension (HPH) rats and investigate the underlying mechanism. Sixty male Sprague-Dawley (SD) rats were divided into control, hypoxia, and hypoxia + Tsantan Sumtang (1.0, 1.25, and 1.5 g•kg•d) groups. Chronic hypoxia was induced by putting the rats inside a hypobaric chamber for four weeks and adjusting the inner pressure and oxygen content to match an altitude of 4500 m. Echocardiography was used to assess RV function and right ventricular-pulmonary arterial (RV-PA) coupling. The physiological parameters of the animals were also evaluated. Morphological characteristics of RV were assessed by hematoxylin and eosin (H&E) staining and TEM. Masson's trichrome staining, immunohistochemical staining, western blotting, and TUNEL assay were used to assess fibrosis and apoptosis levels. The antioxidant and anti-apoptosis properties of Tsantan Sumtang were also evaluated. The effect of Tsantan Sumtang on ROCK signaling pathway was evaluated using real-time quantitative PCR and western blotting. We established an HPH rat model as indicated by the significant increases in the physiological parameters of the rats. Tsantan Sumtang showed a significant cardiac-protective function and an improved effect on RV-PA coupling. Moreover, Tsantan Sumtang treatment inhibited fibrosis and alleviated apoptosis and oxidative stress in RV. In terms of mechanism, Tsantan Sumtang reduced the expression of ROCK (ROCK1, ROCK2) in RV, inhibited cardiac remodeling-related transcription factors (NFATc3, P-STAT3), and regulated apoptosis-related proteins. Tsantan Sumtang was able to restore RV function, improve RV-PA coupling, recover hemodynamic and hematological indexes, and protect RV against structural maladaptive remodeling in the HPH rats. These findings demonstrated that Tsantan Sumtang protects the function of RV in HPH rats. The antioxidant and anti-apoptosis properties of Tsantan Sumtang may be responsible for inhibiting the ROCK signaling pathway.
Zhanting Yang, Haixia Sun, Shanshan Su, Xingmei Nan, Ke Li, Xueqin Jin, Guoen Jin, Zhanqiang Li, Dianxiang Lu

2419 related Products with: Tsantan Sumtang Restored Right Ventricular Function in Chronic Hypoxia-Induced Pulmonary Hypertension Rats.

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#33525548   2021/01/28 To Up

Serum microRNAs as Tool to Predict Early Response to Benralizumab in Severe Eosinophilic Asthma.

Severe eosinophilic asthma poses a serious health and economic problem, so new therapy approaches have been developed to control it, including biological drugs such as benralizumab, which is a monoclonal antibody that binds to IL-5 receptor alpha subunit and depletes peripheral blood eosinophils rapidly. Biomarkers that predict the response to this drug are needed so that microRNAs (miRNAs) can be useful tools. This study was performed with fifteen severe eosinophilic asthmatic patients treated with benralizumab, and serum miRNAs were evaluated before and after treatment by semi-quantitative PCR (qPCR). Patients showed a clinical improvement after benralizumab administration. Additionally, deregulation of miR-1246, miR-5100 and miR-338-3p was observed in severe asthmatic patients after eight weeks of therapy, and a correlation was found between miR-1246 and eosinophil counts, including a number of exacerbations per year in these severe asthmatics. In silico pathway analysis revealed that these three miRNAs are regulators of the MAPK signaling pathway, regulating target genes implicated in asthma such as , , , , and . In this study, we observed an altered expression of miR-1246, miR-5100 and miR-338-3p after eight weeks of benralizumab administration, which could be used as early response markers.
José A Cañas, Marcela Valverde-Monge, José M Rodrigo-Muñoz, Beatriz Sastre, Marta Gil-Martínez, Raquel García-Latorre, Manuel J Rial, Aida Gómez-Cardeñosa, Mar Fernández-Nieto, Erwin J Pinillos-Robles, María J Rodríguez-Nieto, Nicolás González-Mangado, Joaquín Sastre, Victoria Del Pozo

1962 related Products with: Serum microRNAs as Tool to Predict Early Response to Benralizumab in Severe Eosinophilic Asthma.

1 kit1 kit1 module1 module102 modules2 modules1 module1 kit(96 Wells)

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#33520407   2021/01/11 To Up

NFATc3 inhibits hepatocarcinogenesis and HBV replication via positively regulating RIG-I-mediated interferon transcription.

Nuclear factor of activated T cells 3 (NFATc3) has been reported to upregulate type I interferons (IFNs) expression, and the abnormal expression and activation of NFATc3 were closely related to tumorigenesis. However, the potential function of NFATc3 in hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) remains to be elucidated. In this study, we found that NFATc3 gene was frequently deleted and downregulated in HCC tumor tissues, and that the downregulation of NFATc3 was associated with poor prognosis of HCC patients. The gain- and loss-of-function experiments demonstrated that NFATc3 inhibited HCC cell proliferation and invasion, as well as HBV replication. Mechanistically, NFATc3 could bind to the promoters of IFNL1 and IFNB1 genes and prompt the production of IFNs and interferon-stimulated genes. Furthermore, retinoic acid-inducible gene-I (RIG-I) pathway activation increased NFATc3 expression and nuclear localization, and activated NFATc3 further enhanced RIG-I-mediated IFN responses. Collectively, our findings reveal a novel regulatory signaling cascade, the RIG-I/NFATc3/IFNs axis, which inhibits hepatocarcinogenesis and HBV replication by enhancing the immune response in hepatocytes, and this functional axis might potentially be exploited for therapeutic benefits in the clinical treatment of HBV-related HCC.
Xiaobin Zao, Jin Cheng, Congle Shen, Guiwen Guan, Xiaoyu Feng, Jun Zou, Jing Zhang, Tianxu Liu, Huiling Zheng, Ting Zhang, Jie Wang, Jia Liu, Deyao Li, Fengmin Lu, Fuping You, Xiangmei Chen

1609 related Products with: NFATc3 inhibits hepatocarcinogenesis and HBV replication via positively regulating RIG-I-mediated interferon transcription.

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#33495839   2021/01/26 To Up

MicroRNA‑153 attenuates hypoxia‑induced excessive proliferation and migration of pulmonary arterial smooth muscle cells by targeting ROCK1 and NFATc3.

The aim of the present study was to explore the effect of microRNA (miR)‑153 on the proliferation and migration of pulmonary artery smooth muscle cells (PASMCs) in a hypoxic condition by targeting ρ‑associated, coiled‑coil‑containing protein kinase 1 (ROCK1) and nuclear factor of activated T cells cytoplasmic 3 (NFATc3). The right ventricular systolic pressure, right ventricular hypertrophy index, medial wall thickness and medial wall area were studied at different time‑points after rats were exposed to hypoxia. Western blot analysis was used to detect ROCK1 and NFATc3 protein levels. In addition, reverse transcription‑quantitative (RT‑q) PCR was performed to confirm the mRNA levels of miR‑153, ROCK1 and NFATc3 in human (H)PASMCs under hypoxic conditions. Transfected cells were then used to evaluate the effect of miR‑153 on cell proliferation and migration abilities. The association between miR‑153 and ROCK1 or NFATc3 was identified through double luciferase assays. Hypoxia induced pulmonary vascular remodeling and pulmonary arterial hypertension, which resulted from the abnormal proliferation of HPASMCs. ROCK1 and NFATc3 were the target genes of miR‑153 and miR‑153 mimic inhibited the protein expressions of ROCK1 and NFATc3 in HPASMCs and further inhibited cell proliferation and migration under hypoxic conditions. By contrast, the miR‑153 inhibitor promoted the proliferation and migration of HPASMCs. miR‑153 regulated the proliferation and migration of HPASMCs under hypoxia by targeting ROCK1 and NFATc3.
Minjie Zhao, Wei Wang, Ya Lu, Nan Wang, Delei Kong, Lina Shan

2205 related Products with: MicroRNA‑153 attenuates hypoxia‑induced excessive proliferation and migration of pulmonary arterial smooth muscle cells by targeting ROCK1 and NFATc3.

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#33450402   2021/01/12 To Up

Kinase-substrate Edge Biomarkers Provide A More Accurate Prognostic Prediction in ER-negative Breast Cancer.

The estrogen receptor (ER)-negative breast cancer subtype is aggressive with few treatment options available. To identify specific prognostic factors for ER-negative breast cancer, this study included 705,740 and 1034 breast invasive cancer patients from the Surveillance, Epidemiology, and End Results (SEER) and The Cancer Genome Atlas (TCGA) databases, respectively. To identify key kinase-substrate node and edge biomarkers between ER-negative and ER-positive breast cancer patients, we adopted a network-based method using correlation coefficients between molecular pairs in the kinase regulatory network. Integrated analysis of the clinical and molecular data revealed the significant prognostic power of kinase-substrate node and edge features for both subtypes of breast cancer. Two promising kinase-substrate edge features, CSNK1A1-NFATC3 and SRC-OCLN, were identified for more accurate prognostic prediction in ER-negative breast cancer patients.
Yidi Sun, Chen Li, Shichao Pang, Qianlan Yao, Luonan Chen, Yixue Li, Rong Zeng

2062 related Products with: Kinase-substrate Edge Biomarkers Provide A More Accurate Prognostic Prediction in ER-negative Breast Cancer.



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#33393109   2021/01/03 To Up

Calcineurin A gamma and NFATc3/SRPX2 axis contribute to human embryonic stem cell differentiation.

Our understanding of signaling pathways regulating the cell fate of human embryonic stem cells (hESCs) is limited. Calcineurin-NFAT signaling is associated with a wide range of biological processes and diseases. However, its role in controlling hESC fate remains unclear. Here, we report that calcineurin A gamma and the NFATc3/SRPX2 axis control the expression of lineage and epithelial-mesenchymal transition (EMT) markers in hESCs. Knockdown of PPP3CC, the gene encoding calcineurin A gamma, or NFATC3, downregulates certain markers both at the self-renewal state and during differentiation of hESCs. Furthermore, NFATc3 interacts with c-JUN and regulates the expression of SRPX2, the gene encoding a secreted glycoprotein known as a ligand of uPAR. We show that SRPX2 is a downstream target of NFATc3. Both SRPX2 and uPAR participate in controlling expression of lineage and EMT markers. Importantly, SRPX2 knockdown diminishes the upregulation of multiple lineage and EMT markers induced by co-overexpression of NFATc3 and c-JUN in hESCs. Together, this study uncovers a previously unknown role of calcineurin A gamma and the NFATc3/SRPX2 axis in modulating the fate determination of hESCs.
Hao Chen, Yanwu Zeng, Min Shao, Hanzhi Zhao, Zhuoqing Fang, Junjie Gu, Bing Liao, Ying Jin

2799 related Products with: Calcineurin A gamma and NFATc3/SRPX2 axis contribute to human embryonic stem cell differentiation.

24 wells5 x 50 ug50 ug 100ul100 μg100 1.00 flask200 96 wells (1 kit)5100 μg 100ul

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#33356397   2020/12/28 To Up

Magnesium Supplementation Attenuates Pulmonary Hypertension via Regulation of Magnesium Transporters.

Pulmonary hypertension (PH) is characterized by profound vascular remodeling and altered Ca homeostasis in pulmonary arterial smooth muscle cells (PASMCs). Magnesium ion (Mg), a natural Ca antagonist and a cofactor for numerous enzymes, is crucial for regulating diverse cellular functions, but its roles in PH remains unclear. Here, we examined the roles of Mg and its transporters in PH development. Chronic hypoxia and monocrotaline induced significant PH in adult male rats. It was associated with a reduction of [Mg] in PASMCs, a significant increase in gene expressions of , , , , , , , , , and ; upregulation of SLC41A1, SLC41A2, CNNM2, and TRPM7 proteins; and downregulation of SLC41A3 mRNA and protein. Mg supplement attenuated pulmonary arterial pressure, right heart hypertrophy, and medial wall thickening of pulmonary arteries, and reversed the changes in the expression of Mg transporters. Incubation of PASMCs with a high concentration of Mg markedly inhibited PASMC proliferation and migration, and increased apoptosis, whereas a low level of Mg produced the opposite effects. siRNA targeting attenuated PASMC proliferation and migration, but promoted apoptosis; and overexpression also caused similar effects. Moreover, siRNA targeting or high [Mg] incubation inhibited hypoxia-induced upregulation and nuclear translocation of NFATc3 in PASMCs. The results, for the first time, provide the supportive evidence that Mg transporters participate in the development of PH by modulating PASMC proliferation, migration, and apoptosis; and Mg supplementation attenuates PH through regulation of Mg transporters involving the NFATc3 signaling pathway.
Dan Wang, Zhuang-Li Zhu, Da-Cen Lin, Si-Yi Zheng, Kun-Han Chuang, Long-Xin Gui, Ru-Hui Yao, Wei-Jie Zhu, James S K Sham, Mo-Jun Lin

2897 related Products with: Magnesium Supplementation Attenuates Pulmonary Hypertension via Regulation of Magnesium Transporters.

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#33346797   // To Up

Upregulated LRRC55 promotes BK channel activation and aggravates cell injury in podocytes.

Podocyte injury is a common hallmark in various glomerular diseases. The level of LRRC55 was increased in podocytes of patients with focal segmental glomerulosclerosis (FSGS), diabetic nephropathy (DN), and membranous nephropathy (MN). Upregulated LRRC55 and increased intracellular Ca2+ led to BK channel activation and the loss of intracellular potassium, resulting in apoptosome formation and caspase-3 activation in angiotensin II (Ang II)-treated podocytes. Knockout of Lrrc55 or the BK channel prevented the BK current and ameliorated podocyte injury in Ang II-treated mice. Upstream, NFATc3 regulated the expression of LRRC55. Increased LRRC55 expression in podocytes was also evident in animal models of FSGS, DN, and MN. Treatment with losartan or LRRC55 siRNA suppressed LRRC55 expression, prevented BK channel activation, and attenuated podocyte injury in animal models of FSGS, DN, and MN. In conclusion, upregulated LRRC55 promotes BK channel activation and aggravates cell injury in podocytes in FSGS, DN, and MN. LRRC55 inhibition may represent a new therapeutic approach for podocyte injury.
Shuai Hu, Runhong Han, Long Chen, Weisong Qin, Xiaodong Xu, Jingsong Shi, Xiaodong Zhu, Mingchao Zhang, Caihong Zeng, Zheng Tang, Hao Bao, Zhihong Liu

2941 related Products with: Upregulated LRRC55 promotes BK channel activation and aggravates cell injury in podocytes.

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#33283362   2020/12/22 To Up

Concomitant overexpression of mir-182-5p and mir-182-3p raises the possibility of IL-17-producing Treg formation in breast cancer by targeting CD3d, ITK, FOXO1, and NFATs: A meta-analysis and experimental study.

T cells are polarized toward regulatory T cells (Tregs) in tumor microenvironment by the shuttling of microRNAs that target T cell-activating signaling pathways. We evaluated the expression of the miR-182 cluster (miR-96, 182, and 183) in peripheral blood mononuclear cells (PBMCs) of patients with breast cancer (BC), and T cell polarization by the expression of FOXO1, NFATs, ITK, TCR/CD3 complex, and IL-2/IL-2RA. Twenty-six microRNAs overexpressed in tumor tissues and sera of these patients were extracted by a meta-analysis. Then, the expression of the miR-182 cluster was investigated in PBMCs and sera of these patients and correlated with their targets in PBMCs. Finally, miR-182 was cloned into Jurkat cells to evaluate its effects on T cell polarization. FOXO1, CD3d, ITK, NFATc3, NFATc4, and IL-2RA were targeted by miR-182, due to which their expression decreased in PBMCs of patients. Although IL-6, IL-17, and TGF-β increased after miR-182 transduction, IL-2 dramatically decreased. We revealed CD4 FOXP3 T cell differentiation in the miR-182-transduced group. Although miR-182 has inhibitory effects on T cells by the inhibition of FOXO1, TCR/CD3 complex, NFATs, and IL-2/IL-2RA signaling pathways, it increases FOXP3, TGF-β, and IL-17 expression to possibly drive T cell deviation toward the transitional state of IL-17-producing Tregs and Treg formation in the end.
Mohammad Hasan Soheilifar, Hajar Vaseghi, Farhad Seif, Mehdi Ariana, Shima Ghorbanifar, Nazanin Habibi, Fatemeh Papari Barjasteh, Majid Pornour

1604 related Products with: Concomitant overexpression of mir-182-5p and mir-182-3p raises the possibility of IL-17-producing Treg formation in breast cancer by targeting CD3d, ITK, FOXO1, and NFATs: A meta-analysis and experimental study.

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#33246743   2020/11/24 To Up

LncRNA NRON promotes M2 macrophage polarization and alleviates atrial fibrosis through suppressing exosomal miR-23a derived from atrial myocytes.

miR-23a is a pro-hypertrophic miRNA that inhibits M2 macrophage polarization. A previous study demonstrated that lncRNA NRON alleviated atrial fibrosis through suppression of M1 macrophages activated by atrial myocytes. This study aimed to determine whether NRON promotes M2 macrophage polarization and alleviates atrial fibrosis through suppressing exosomal miR-23a derived from atrial myocytes.
Jianan Li, Qingchun Zhang, Haimiao Jiao

1428 related Products with: LncRNA NRON promotes M2 macrophage polarization and alleviates atrial fibrosis through suppressing exosomal miR-23a derived from atrial myocytes.

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