Estradiol differentially regulates calreticulin: a potential link with abnormal T cell function in systemic lupus erythematosus?
Estradiol differentially regulates calreticulin: a potential link with abnormal T cell function in systemic lupus erythematosus?
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DOI：
10.1177/0961203313482742
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发表时间：
2013-05
期刊：
影响因子：
2.6
通讯作者：
Kimler B
中科院分区：
文献类型：
--
作者：
Ward JM;Rider V;Abdou NI;Kimler B
系统性红斑狼疮(SLE)是一种自身免疫性疾病，女性患病的频率是男性的九倍。本研究探讨雌激素对钙缓冲蛋白钙网蛋白的调节作用，以进一步了解SLE T细胞异常T细胞信号的分子基础。从健康女性和SLE患者的血液样本中提纯T细胞。用实时定量聚合酶链式反应检测钙网蛋白的表达。将钙网蛋白和雌激素受体-α共沉淀，用Western blotting分析这两种蛋白是否与T细胞相关。在激活的对照T细胞中，钙网织蛋白的表达增加(p=0.034)，而在静止T细胞中，雌二醇的表达减少(p=0.044)。在活化的SLE T细胞样本中，钙网蛋白的表达减少，而在大约50%的静息T细胞样本中表达增加。SLE患者和正常志愿者的血浆雌二醇水平相似(p>；0.05)。雌激素受体-α和钙网蛋白从胞核和胞浆中共沉淀出来。结果表明，雌二醇对正常人T细胞钙网蛋白的表达有较强的调节作用，且激活T细胞和静止T细胞的动态变化不同。SLE T细胞缺乏这种严密的调节可能导致T细胞功能异常。
Systemic lupus erythematosus (SLE) is an autoimmune disease that affects women nine times more often than men. The present study investigates estradiol-dependent control of the calcium buffering protein, calreticulin, to gain further insight into the molecular basis of abnormal T cell signaling in SLE T cells. T cells were purified from blood samples obtained from healthy females and SLE patients. Calreticulin expression was quantified by real time polymerase chain amplification. Calreticulin and estrogen receptor-α were co-precipitated and analyzed by Western blotting to determine if the proteins associate in T cells. Calreticulin expression increased (p= 0.034)in activated control T cells, while estradiol decreased (p = 0.044) calreticulin in resting T cells. Calreticulin expression decreased in activated SLE T cell samples and increased in approximately 50% of resting T cell samples. Plasma estradiol was similar (p > 0.05) among SLE patients and control volunteers. Estrogen receptor-αand calreticulin co-precipitated from nuclear and cytoplasmic T cell compartments. The results indicate that estradiol tightly regulates calreticulin expression in normal human T cells and the dynamics are different between activated and resting T cells. The absence of this tight regulation in SLE T cells could contribute to abnormal T cell function.
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影响因子：
7.3
作者：
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通讯作者：
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影响因子：
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影响因子：
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作者：
Fu, Hongmei;Liu, Changzhen;Gao, Bin
通讯作者：
Gao, Bin
影响因子：
--
作者：
Heldring, Nina;Isaacs, Gary D.;Kraus, W. Lee
通讯作者：
Kraus, W. Lee