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find Keyword "细胞活化" 8 results
  • 敲除与Th2 细胞活化相关的电压依赖钙通道可防止实验性哮喘发生(Knocking down Cav1 calcium channels implicated in Th2 cell activation prevents experimental asthma)

    敲除与Th2 细胞活化相关的电压依赖钙通道可防止实验性哮喘发生(Knocking down Cav1 calcium channels implicated in Th2 cell activation prevents experimental asthma) 【摘要翻译】 研究理由: Th2 型细胞参与过敏性哮喘,这些细胞产生的细胞因子( IL-4、IL-5 及IL-13) 在过敏状态时分泌增加。因此, 研究Th2 型细胞表达的对其功能具有重要影响的关键信号分子至关重要。我们既往的研究显示二氢吡¤特异性调控Th2 细胞的功能。目的: 由于二氢吡¤可特异性与活化细胞的电压依赖钙通道( Cav1) 结合并调节其功能, 我们的主要目的是证实Th2 细胞特异性表达功能性的Cav1 相关通道, 抑制其功能可能抑制哮喘。方法: 我们通过定量PCR 和Western blot 检测Th2 和Th1 细胞Cav1 通道表达。我们将Th2 细胞表达的Cav1 的异构体进行测序, 并研究Cav1 反义寡核苷酸( Cav1AS) 是否影响Ca2 + 信号及细胞因子的产生。最后, 我们通过给OVA 鼻腔激发的BALB/c小鼠注射Cav1AS 转染的OVA 特异性Th2 细胞研究Cav1AS在被动免疫哮喘动物模型中的作用, 并通过鼻腔给予此前进行过OVA 及氢氧化铝免疫的BABL/ c 小鼠Cav1AS 和OVA溶液以研究Cav1AS 对主动免疫哮喘模型的影响。检测和主要结果: 我们发现小鼠Th2 细胞而非Th1 细胞表达Cav1. 2和Cav1. 3 通道。转染Cav1AS 抑制了钙通路和细胞因子产生, 并导致Th2 细胞丧失过继Th2 细胞诱导气道炎症功能。鼻腔内给予Cav1AS 可抑制主动免疫导致的哮喘气道炎症和气道高反应性。结论: 这些结果提示Th2 细胞特异性表达Cav1. 2 and Cav1. 3 通道, 以此作为治疗靶点可有效抑制动物模型的哮喘反应。 【述评】 哮喘是一种Th2 型慢性气道炎症反应疾病,目前机制未明。Th2 细胞在此过程中发挥关键作用, 但Th2细胞活化机制不清楚。本文的研究发现Th2 细胞特异性表达Cav1. 2 和Cav1. 3 通道, 以Cav1AS抑制Cav1 通道的表达可抑制Th2 细胞功能进而抑制哮喘炎症反应。该研究揭示了哮喘气道炎症反应的新机制, 为哮喘治疗提供了新靶点。但是, Cav1 通道如何影响Th2 细胞的功能尚需进一步研究。其次, 有些基因在人类和小鼠表达并不一致, 特别是一些异构体的表达水平不同, 甚至在功能上存在很大差异, 因此, 在哮喘患者中Cav1 通道的表达尚待研究。最后, Th2 功能失调在一些自身免疫性疾病中发挥重要作用, 因此, 如证实Cav1 通道可用于人类哮喘治疗, 则该方法可能对其他一些自身免疫性疾病有治疗作用。

    Release date:2016-08-30 11:54 Export PDF Favorites Scan
  • 成纤维细胞活化蛋白在上皮癌中表达的意义及研究进展

    【摘要】 成纤维细胞活化蛋白(fibroblast activation protein,FAP)广泛存在于上皮癌组织中,在肿瘤间质成纤维细胞选择性表达而在正常的成熟组织中几乎不表达,是上皮癌的特异性靶标。FAP具有蛋白酶活性,并且可与其他细胞表面蛋白分子形成复合物,可能作用于细胞信号传导,参与肿瘤间质重塑和血管网的形成,调节肿瘤细胞的生长、分化、黏附和转移。目前,有许多临床前期实验及临床研究报导,靶向FAP能有效抑制上皮癌的生长和转移。FAP将可能成为治疗上皮癌的新靶点。现综述总结了FAP的生物学特性,其表达对上皮癌发生发展的影响,以及靶向FAP的抗肿瘤研究进展。

    Release date:2016-09-08 09:26 Export PDF Favorites Scan
  • Activation of Adenosine 2A Receptor Inhibiting Rat T Cell Function in Vitro

    Objective To study the effects of adenosine 2A receptor activation on activation, proliferation, and toxicity of T lymphocytes stimulated by phytohemagglutinin (PHA) in vitro. Methods A model of activated T cells was established by stimulating the cells with PHA. Those T cells were treated with different concentrations of adenosine 2A receptors agonist (0.01 μmol/L, 0.1 μmol/L, 1 μmol/L, and 10 μmol/L CGS21680). The expressions of CD69, CD25 and proliferation of T cells were measured by fluorescent antibody stain and flow cytometry. ELISA method was used to detect IL-2 and INF-γ levels. Results All concentrations of CGS21680 significantly inhibited the expressions of CD25 and CD69 on PHA-stimulated T cells surface and proliferation of T cells (Plt;0.05, Plt;0.01). IL-2 and INF-γ secreted by T cells were significantly suppressed, too (Plt;0.01). Conclusion Activation of adenosine 2A receptor can effectively inhibit the activation, proliferation, and toxicity of T cells in vitro.

    Release date:2016-09-08 10:50 Export PDF Favorites Scan
  • Research progress of pancreas stellate cells in pancreas fibrosis

    Objective To review research progress of pancreas stellate cells in pancreas fibrosis and understand characteristics and activation of pancreas stellate cells and its mechanism on pancreas fibrosis. Method The relevant literatures about pancreas stellate cells and its studies in pancreas fibrosis were reviewed. Results The activation of pancreatic stellate cell is associated with fibrosis of pancreatitis and end stage of pancreas transplantation, but its effect and regulation mechanisms for the extracelluar and intracellular molecular network need to be further investigated. Conclusion Elucidation of activation of pancreas stellate cells will facilitate understanding of pancreas fibrosis and searching new target in treatment of pancreas fibrosis.

    Release date:2017-05-04 02:26 Export PDF Favorites Scan
  • The potential role of calnexin in the activation of cardiac fibroblasts

    Calnexin is a lectin-like molecular chaperone protein on the endoplasmic reticulum, mediating unfolded protein responses, the endoplasmic reticulum Ca2+ homeostasis, and Ca2+ signals conduction. In recent years, studies have found that calnexin plays a key role in the heart diseases. This study aims to explore the role of calnexin in the activation of cardiac fibroblasts. A transverse aortic constriction (TAC) mouse model was established to observe the activation of cardiac fibroblasts in vivo, and the in vitro cardiac fibroblasts activation model was established by transforming growth factor β1 (TGFβ1) stimulation. The adenovirus was respectively used to gene overexpression and silencing calnexin in cardiac fibroblasts to elucidate the relationship between calnexin and cardiac fibroblasts activation, as well as the possible underlying mechanism. We confirmed the establishment of TAC model by echocardiography, hematoxylin-eosin, Masson, and Sirius red staining, and detecting the expression of cardiac fibrosis markers in cardiac tissues. After TGFβ1 stimulation, markers of the activation of cardiac fibroblast, and proliferation and migration of cardiac fibroblast were detected by quantitative PCR, Western blot, EdU assay, and wound healing assay respectively. The results showed that the calnexin expression was reduced in both the TAC mice model and the activated cardiac fibroblasts. The overexpression of calnexin relieved cardiac fibroblasts activation, in contrast, the silencing of calnexin promoted cardiac fibroblasts activation. Furthermore, we found that the endoplasmic reticulum stress was activated during cardiac fibroblasts activation, and endoplasmic reticulum stress was relieved after overexpression of calnexin. Conversely, after the silencing of calnexin, endoplasmic reticulum stress was further aggravated, accompanying with the activation of cardiac fibroblasts. Our data suggest that the overexpression of calnexin may prevent cardiac fibroblasts against activation by alleviating endoplasmic reticulum stress.

    Release date:2020-08-21 07:07 Export PDF Favorites Scan
  • The potential role of long non-coding RNA Dnm3os in the activation of cardiac fibroblasts

    Long non-coding RNA (lncRNA) Dnm3os plays a critical role in peritendinous fibrosis and pulmonary fibrosis, but its role in the process of cardiac fibrosis is still unclear. Therefore, we carried out study by using the myocardial fibrotic tissues obtained by thoracic aortic constriction (TAC) in an early study of our group, and the in vitro cardiac fibroblast activation model induced by transforming growth factor-β1 (TGF-β1). Quantitative real-time polymerase chain reaction (RT-qPCR), Western blot, and collagen gel contraction test were used to identify the changes of activation phenotype and the expression of Dnm3os in cardiac fibroblasts. Small interfering RNA was used to silence Dnm3os to explore its role in the activation of cardiac fibroblasts. The results showed that the expression of Dnm3os was increased significantly in myocardial fibrotic tissues and in the activated cardiac fibroblasts. And the activation of cardiac fibroblasts could be alleviated by Dnm3os silencing. Furthermore, the TGF-β1/Smad2/3 pathway was activated during the process of cardiac fibroblasts activation, while was inhibited after silencing Dnm3os. The results suggest that Dnm3os silencing may affect the process of cardiac fibroblast activation by inhibiting TGF-β1/Smad2/3 signal pathway. Therefore, interfering with the expression of lncRNA Dnm3os may be a potential target for the treatment of cardiac fibrosis.

    Release date:2021-06-18 04:52 Export PDF Favorites Scan
  • 急性 Q 热继发巨噬细胞活化一例

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  • Role and mechanism of peroxisome proliferator-activated receptor gamma coactivator 1α in inhibiting aortic valve interstitial cell activation

    Objective To investigate the role and mechanism of peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α) in the activation of aortic valve interstitial cells (AVICs) in aortic stenosis. Methods Isolating primary AVICs and stimulating their activation with transforming growth factor β1 (TGF-β1, 30 ng/mL), the expression of PGC-1α was detected. The activation of AVICs induced by TGF-β1 was observed after overexpression of PGC-1α by adenovirus or inhibition of PGC-1α function by GW9662. The possible downstream molecular mechanism of PGC-1α in AVICs activation was screened. Finally, the phenotype was further verified in primary human AVICs. Results The expression of PGC-1α decreased after the activation of AVICs induced by TGF-β1 (control group: 1.00±0.18; 24 h: 0.31±0.10; 48 h: 0.32±0.06; 72 h: 0.20±0.07; P<0.05). Specific overexpression of PGC-1α by adenovirus inhibited the activation of AVICs induced by TGF-β1 stimulation (periostin: 3.17±0.64 vs. 1.45±0.54, P<0.05; α-smooth muscle actin: 0.77±0.11 vs. 0.28±0.06, P<0.05). On the contrary, inhibition of PGC-1α function by GW9662 promoted the activation of AVICs (periostin: 2.20±0.68 vs. 7.99±2.50, P<0.05). Subsequently, it was found that PGC-1α might inhibit the activation of AVICs through downregulating the expression of calcium/calmodulin-dependent protein kinase (CAMK1δ) (0.97±0.04 vs. 0.74±0.11, P<0.05), and downregulating the expression of CAMK1δ alleviated the activation of AVICs (periostin: 1.76±0.11 vs. 0.99±0.20, P<0.05). The possible mechanism was that the activation of mammalian target of rapamycin (mTOR) signaling pathway was inhibited by reducing the accumulation of reactive oxygen species (ROS) (778.3±139.4 vs. 159.3±43.2, P<0.05). Finally, the protective effect of PGC-1α overexpression was verified in the activated phenotype of human AVICs (periostin: 2.73±0.53 vs. 1.63±0.14, P<0.05; connective tissue growth factor: 1.27±0.04 vs. 0.48±0.09, P<0.05). Conclusions The expression of PGC-1α significantly decreases during the activation of AVICs induced by TGF-β1. The overexpression of PGC-1α significantly inhibites the activation of AVICs, suggesting that PGC-1α plays a protective role in the activation of AVICs. The possible mechanism is that PGC-1α can inhibit the activation of CAMK1δ-ROS-mTOR pathway. In conclusion, interventions based on PGC-1α expression levels are new potential therapeutic targets for aortic stenosis.

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