Gu J, et al. Arthritis Rheum. 2009;60(11):3269-79.
del.icio.us 标签: 中信国健临床通讯，G蛋白调节子，RGS1，未分化脊柱关节炎，uSpA，生物学标记，外周血单个核细胞，PBMCs
目的：比较伴有炎性下腰痛的AS病人和未分化脊柱关节炎(uSpA)病人之间的基因表达谱差异。 方法：采集AS、uSpA以及健康志愿者的外周血单个核细胞(PBMCs)，采用基因芯片技术进行基因筛选，之后采用实时PCR验证筛选所得。结果：基因表达谱数据和实时PCR分析显示，AS病人和健康志愿者之间差异细微。相对而言，uSpA病人显著更高表达20个基因。G蛋白调节子1 (RGS1)是区分uSpA与对照组的最有用生物学标记，对于区分AS病人与对照组也有一定的作用(P值分别为2.3 x 10(-7)以及6.7 x 10(-3))。验证工作在另一独立的病人群中进行，包括RA病人以及机械性腰背痛病人。在第一、第二组uSpA病人中接收者工作特征(ROC)的曲线下面积分别为0.99和0.93(P = 1 x 10(-4))。为了评价RGS1的可能来源，我们用一组细胞因子和趋化因子培养了一种单核细胞来源的细胞系。TNF-a或者IL-17均可明显诱导表达RGS1。结论：本研究显示，与AS病人或者健康者相比，uSpA病人PBMCs显著更高表达某些基因，而且TNF-a和IL-17诱导的RGS1是鉴别伴有炎性下腰痛的uSpA的潜在生物学标记，对区分伴有炎症性下腰痛的AS病人与健康对照人群也有一定的作用。
Arthritis Rheum. 2009 Nov;60(11):3269-79.
Identification of RGS1 as a candidate biomarker for undifferentiated spondylarthritis by genome-wide expression profiling and real-time polymerase chain reaction.
Gu J, Wei YL, Wei JC, Huang F, Jan MS, Centola M, Frank MB, Yu D.
Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
OBJECTIVE: To compare gene expression profiles between ankylosing spondylitis (AS) and undifferentiated spondylarthritis (uSpA) patients with inflammatory low back pain. METHODS: Peripheral blood mononuclear cells (PBMCs) from patients with AS, patients with uSpA, and healthy subjects were screened using genome-wide microarrays, followed by validation by real-time polymerase chain reaction (PCR). RESULTS: Microarray profiling and real-time PCR assays showed only minor differences between AS patients and healthy subjects. In contrast, 20 genes were strikingly more highly expressed in uSpA patients. Regulator of G protein signaling 1 (RGS1) was identified as the most useful biomarker for distinguishing uSpA patients, and to a lesser extent AS patients, from control subjects (P = 2.3 x 10(-7) and 6.7 x 10(-3), respectively). These findings were verified in an independent cohort that also included patients with rheumatoid arthritis and patients with mechanical low back pain. The receiver operating characteristic area under the curve values in the first and second cohorts of uSpA patients were 0.99 and 0.93, respectively (P = 1 x 10(-4)). To evaluate the possible derivation of RGS1, we cultured a monocyte-derived cell line with a panel of cytokines and chemokines. RGS1 was significantly induced either by tumor necrosis factor alpha (TNFalpha) or by interleukin-17 (IL-17). CONCLUSION: Our findings indicate that uSpA PBMCs carry strikingly more highly expressed genes compared with PBMCs from AS patients or healthy subjects, and that TNFalpha- and IL-17-inducible RGS1 is a potential biomarker for uSpA, and to a lesser extent for AS, with inflammatory low back pain.