Lamana Amalia, López-Santalla Mercedes, Castillo-González Raquel, Ortiz Ana María, Martín Javier, García-Vicuña Rosario, González-Álvaro Isidoro
Servicio de Reumatología, Hospital Universitario de la Princesa, Instituto de Investigación Sanitaria Hospital Universitario La Princesa, Madrid, Spain.
Departamento de Inmunología y Oncología, Centro Nacional de Biotecnología, CSIC, Madrid, Spain.
PLoS One. 2015 Nov 16;10(11):e0142683. doi: 10.1371/journal.pone.0142683. eCollection 2015.
The T allele of rs7574865 in STAT4 confers risk of developing autoimmune disorders. However, its functional significance remains unclear. Here we analyze how rs7574865 affects the transcription of STAT4 and its protein expression.
We studied 201 patients (80% female; median age, 54 years; median disease duration, 5.4 months) from PEARL study. Demographic, clinical, laboratory and therapeutic data were collected at each visit. IL-6 serum levels were measured by enzyme immune assay. The rs7574865 was genotyped using TaqMan probes. The expression levels of STAT4 mRNA were determined at 182 visits from 69 patients using quantitative real-time polymerase chain reaction. STAT4 protein was assessed by western blot in 62 samples from 34 patients. To determine the effect of different variables on the expression of STAT4 mRNA and protein, we performed multivariate longitudinal analyses using generalized linear models.
After adjustment for age, disease activity and glucocorticoid dose as confounders, the presence of at least one copy of the T allele of rs7574865 was significantly associated with higher levels of STAT4 mRNA. Similarly, TT patients showed significantly higher levels of STAT4 protein than GG patients. IL-6 induced STAT4 and STAT5 phosphorylation in peripheral blood lymphocytes. Patients carrying at least one T allele of rs7574865 displayed lower levels of serum IL-6 compared to GG homozygous; by contrast the production of C-reactive protein was similar in both populations.
Our data suggest that the presence of the rs7574865 T allele enhances STAT4 mRNA transcription and protein expression. It may enhance the signaling of molecules depending on the STAT4 pathway.
信号转导和转录激活因子4(STAT4)基因rs7574865位点的T等位基因会增加自身免疫性疾病的发病风险。然而,其功能意义仍不清楚。在此,我们分析rs7574865如何影响STAT4的转录及其蛋白表达。
我们研究了来自PEARL研究的201例患者(80%为女性;中位年龄54岁;中位病程5.4个月)。每次就诊时收集人口统计学、临床、实验室和治疗数据。采用酶免疫测定法检测血清白细胞介素-6(IL-6)水平。使用TaqMan探针进行rs7574865基因分型。采用定量实时聚合酶链反应在69例患者的182次就诊中测定STAT4信使核糖核酸(mRNA)的表达水平。通过蛋白质印迹法在34例患者的62份样本中评估STAT4蛋白。为了确定不同变量对STAT4 mRNA和蛋白表达的影响,我们使用广义线性模型进行多变量纵向分析。
在校正年龄、疾病活动度和糖皮质激素剂量等混杂因素后,rs7574865的T等位基因至少有一个拷贝与较高水平的STAT4 mRNA显著相关。同样,携带TT基因型的患者STAT4蛋白水平显著高于携带GG基因型的患者。IL-6在外周血淋巴细胞中诱导STAT4和信号转导和转录激活因子5(STAT5)磷酸化。与GG纯合子相比,携带rs7574865至少一个T等位基因的患者血清IL-6水平较低;相比之下,两个群体中C反应蛋白的产生相似。
我们的数据表明,rs7574865 T等位基因的存在增强了STAT4 mRNA转录和蛋白表达。它可能增强依赖于STAT4途径的分子信号传导。