Rong-Hua Song

Shanghai Jiao Tong University, Shanghai, Shanghai Shi, China

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Publications (9)27.22 Total impact

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    ABSTRACT: The objective of this study was to investigate histone modification patterns in peripheral blood mononuclear cells (PBMCs) of patients with Graves' disease (GD). Thirty GD patients and 20 healthy controls were enrolled in this study. Global histone H3/H4 acetylation levels of PBMCs in all subjects were detected by enzyme-linked immunosorbent assay. mRNA levels of histone-related chromatin modifier genes were measured by real-time quantitative reverse transcription-polymerase chain reaction. Global histone H4 acetylation level in PBMCs of GD patients was significantly decreased compared with controls (p=0.005). The mRNA expression of histone deacetylases HDAC1 and HDAC2 were significantly increased in PBMCs of GD patients compared with controls (p=0.004 and 0.018; respectively). No significant difference was observed either in SIRT1 or in HATs mRNA including p300, CREBBP between GD patients and controls (p>0.05). Our findings firstly suggested that histone acetylation modifications are aberrant in PBMCs of GD patients, possibly due to the deregulation of epigenetic modifier genes. Copyright © 2015. Published by Elsevier Ireland Ltd.
    No preview · Article · Jun 2015 · Molecular and Cellular Endocrinology
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    ABSTRACT: The prognosis of Graves' disease (GD) varies among patients. However, the immune pathogenesis of refractory GD is still unknown. The aim of this study was to explore the cytokine expression profile associated with refractory GD. Preliminary cytokine protein microarray screening was performed to detect differentially expressed cytokines in the plasma of 4 refractory GD patients and 4 stable GD patients. Some differentially expressed cytokines were then validated in plasma by enzyme-linked immunosorbent assay (ELISA) and in peripheral blood mononuclear cells (PBMCs) by quantitative real-time polymerase chain reaction (qRT-PCR) on another independent set of samples. We found that 21 cytokines were differentially expressed between intractable GD patients and those in remission, including 18 up- and 3 down-regulated cytokines with a fold change >1.30 and﹤0.77, respectively. Intractability-related elevation of three cytokines (IL-4, IL-6, IL-10) was validated by ELISA in plasma on another GD cohort with 30 patients in recurrence and 14 in remission (t-test, p=0.035, 0.033 and 0.041, respectively). Furthermore, mRNA expression of IL-4, IL-6 and IL-10 in PBMCs, detected by qRT-PCR, was significantly elevated in refractory GD patients compared with those in remission (p=0.039, 0.047 and 0.042, respectively). The severity of GD is associated with the aberrant expression and secretion of several cytokines that may serve as potential biomarkers and predictors for disease prognosis. Targeting these cytokines or their receptors may also lead to a novel therapeutic intervention for GD. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    No preview · Article · Mar 2015 · Clinical Endocrinology
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    ABSTRACT: Abnormal microRNA (miRNA) expression is found in many diseases including autoimmune diseases. However, little is known about the role of miRNA regulation in Graves' disease (GD). Here, we simultaneously detected different expressions of miRNA and mRNAs in thyroid tissues via a high-throughput transcriptomics approach, known as microarray, in order to reveal the relationship between aberrant expression of miRNAs and mRNAs spectrum and GD. Totally 7 specimens of thyroid tissue from 4 GD patients and 3 controls were obtained by surgery for microarray analysis. Then, 30 thyroid specimens (18 GD and 12 controls) were also collected for further validation by quantitative real-time PCR ( qRT-PCR ). Statistical analysis showed that the expressions of 5 specific miRNA were increased significantly while those of other 18 miRNA were decreased in thyroid tissue of GD patients (FC≥1.3 or≤0.77 and p<0.05). In addition, the transcription of 1271 mRNAs was up-regulated, while the expression of 777 mRNAs transcripts was down-regulated (FC≥2.0 or≤0.5 and p<0.05). Furthermore, integrated analysis of differentially expressed miRNA and their target mRNAs demonstrated that 2 miRNA (miR-22 and miR-183) were increased while their potential target mRNAs were decreased. 3 miRNA (miR-101, miR-197 and miR-660) were decreased while their potential target mRNAs were increased. The above findings from microarray screening were confirmed by qRT-PCR in more samples. The results were consistent with those observed in the microarray assays. Our study highlights the possibility that miRNA-target gene network may be involved in the pathogenesis of GD and could provide new insights into understanding the pathophysiological mechanisms of GD. © 2015 S. Karger AG, Basel.
    No preview · Article · Mar 2015 · Cellular Physiology and Biochemistry
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    ABSTRACT: As an autoimmune disease, Graves' disease (GD) is associated with many genetic and environmental risk factors. Although the exact mechanism remains unclear, epigenetic determinants, such as DNA methylation, are thought to contribute to the pathogenesis of GD. Here, we for the first time reported the DNA methylation pattern in GD through a high-throughput analysis. In order to investigate genome-wide DNA methylation profile of GD, Methyl-DNA immunoprecipitation (MeDIP) and Nimblegen human DNA methylation 3×720K promoter plus CpG island microarrays were used to identify differentially methylated regions (DMRs) from blood samples in GD patients. Quantitative methylation-specific PCR (qMSP) was used to validate the methylation state of candidate genes. Transcription level of each gene was estimated by quantitative real-time PCR (qRT-PCR). A total of 132 hypermethylated and 133 hypomethylated regions were identified in GD. The methylation of ICAM1 in GD patients and normal controls was significantly different (P<0.05). In the female group, significantly decreased methylation was observed in GD patients compared with normal controls (P<0.05). The transcription of ICAM1 at the mRNA level was significantly higher in GD patients compared with normal controls (P<0.05). Besides, the transcription of DNMT1 and MECP2 at the mRNA level was significantly decreased in GD patients compared with normal controls (P<0.05). Our findings revealed that the DNA methylation pattern in GD was distinct from that of controls. These results provided new molecular insights into the pathogenesis of GD. Copyright © 2015. Published by Elsevier Inc.
    No preview · Article · Jan 2015 · Genomics
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    ABSTRACT: Our objective was to investigate whether interleukin-1 receptor-associated kinase (IRAK1) and methyl-CpG-binding protein 2 (MECP2) are associated with autoimmune thyroid diseases (AITDs). We selected four single nucleotide polymorphisms (SNPs), rs3027898, rs1059703 in IRAK1 and rs2075596, rs2239464 in MECP2, for genotyping using PCR-based ligase detection reaction (LDR) method in 1042 AITDs patients and 897 controls. Minor alleles in the four SNPs were strongly associated with AITDs, and similar associations were found in Graves' disease (GD). In Hashimoto's thyroiditis (HT) patients, a significantly increased risk of T allele in rs1059703 was found. There were obvious differences in allele and genotype distributions in female AITDs, GD and HT patients. Moreover, the haplotypes CCAA and ATGG were the associated variants for AITDs and GD. Besides, these two haplotypes showed similar associations with AITDs and GD in female patients. Our results firstly indicated that IRAK1 and MECP2 genes are crucial risk factors for AITDs.
    No preview · Article · Dec 2014 · Molecular and Cellular Endocrinology
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    ABSTRACT: Purpose: The aim of this study was to make a comparative analysis of the possible different expression of Th22 cells in two subtypes of autoimmune thyroid diseases (AITDs), i.e., Graves' disease (GD) and Hashimoto's thyroiditis (HT). Methods: We recruited 61 AITDs patients (31 GD and 30 HT) and 22 controls. Serum level of IL-22 was measured by enzyme linked immunosorbent assay (ELISA). The proportion of Th22 cells in peripheral blood mononuclear cells (PBMCs) was analyzed by flow cytometry. The messenger RNA (mRNA) expressions of IL-22, its receptors (IL10R2, IL22R1) and key transcription factor (aryl hydrocarbon receptor, AHR) in PBMCs were assayed by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Several cytokines of the cultured PBMCs were also measured under IL-22 stimulation. Results: The proportion of Th22 cells, serum IL22 level and IL-22 mRNA expression were significantly higher in patients with GD than in healthy controls. Additionally, AHR increased in GD patients compared to healthy controls. However, the elevation of Th22 cells and their relative cytokines was not found in patients with HT. Consistent with specific mRNAs expression of cultured PBMCs, IL-4 increment in supernatant was much higher in GD group than in control group, while IFN-γ levels were decreased under IL-22 stimulation. Conclusion: Th22 cells may participate in the pathogenesis of AITDs as a proinflammatory factor, especially in GD, through expressing and secreting IL-22.
    No preview · Article · Aug 2014 · International journal of clinical and experimental pathology
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    ABSTRACT: Abstract Autoimmune thyroid disease (AITD) is a multifactorial organ-specific autoimmune disorder, and both genetic susceptibility and environmental factors are involved in its etiology. TNFAIP3 encodes the ubiquitin-modifying enzyme (A20), a key regulator of inflammatory signaling pathways. The aim of the present study was to evaluate the association between TNFAIP3 gene polymorphisms and AITD in Chinese Han population. Three single nucleotide polymorphisms (SNPs) in TNFAIP3 gene locus (rs598493, rs610604 and rs661561) were detected in a set of 667 patients with AITD and 301 controls in Han Chinese population using the Matrix Assisted Laser Desorption Ionization-Time of Flight Mass Spectrometer (MALDI-TOF-MS) Platform. Compared with those of the controls, the frequencies of GG genotype of rs598493, the AA genotype of rs610604, the allele G and GG genotype of rs661561 were significantly increased in Graves' disease (GD) patients. However, the frequencies of AG genotype of rs598493 and AC genotype of rs610604 were significantly decreased in GD patients. The ATC haplotype (rs598493, rs661561 and rs610604) was associated with a decreased risk of GD. No significant differences in the three SNPs were observed between HT patients and controls. Our study shows a clear association between the polymorphisms of TNFAIP3 gene and GD, not HT, suggesting that TNFAIP3 gene is likely to be a genetic susceptibility factor to GD.
    No preview · Article · May 2014 · Autoimmunity
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    ABSTRACT: The aim of this study was to investigate the association between signal transducer and activator of transcription 3 (STAT3) polymorphisms and autoimmune thyroid diseases and clinical features. We genotyped six single-nucleotide polymorphisms (SNPs) rs1053005, rs2293152, rs744166, rs17593222, rs2291281, and rs2291282 of STAT3 gene in 667 patients with autoimmune thyroid disease (417 Graves' disease (GD) and 250 Hashimoto's thyroiditis (HT)) and 301 healthy controls. The allele A from rs1053005 was significantly less frequent in both GD and HT patients (P = 0.0024, OR = 0.6958, 95%CI = 0.5508-0.8788; P = 0.0091, OR = 0.7013, 95%CI = 0.5397-0.9112, respectively). The AA genotype of rs1053005 was less in GD and HT patients too (P = 0.0025,OR = 0.6278, 95%CI = 0.466-0.847) and (P = 0.0036,OR = 0.601, 95%CI = 0.428-0.843). The allele G from rs17593222 increased the susceptibility to the ophthalmopathy development both in autoimmune thyroid disease (AITD) and GD patients (P = 0.0007, OR = 3.980, 95%CI = 1.871-8.464; P = 0.0081, OR = 3.378, 95%CI = 1.441-7.919, respectively). The allele A and AA genotype of SNP rs1053005 may protect individuals from the susceptibility to AITD and their frequency decreased in AITD patients. In addition, the allele G of rs17593222 may increase the ophthalmopathy risk in AITD patients. Our findings suggest the existence of association between STAT3 gene and AITD, thus adding STAT3 gene to the list of the predisposing genes to AITD.
    Preview · Article · Oct 2013 · Functional & Integrative Genomics
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    ABSTRACT: Th17 lymphocyte and its relative cytokines have been shown to play an important role in autoimmune thyroid diseases (AITD). The aim of this study was to investigate the association between IL-17A and IL-17F gene polymorphisms and two main types of AITD, Graves' disease (GD) and Hashimoto's thyroiditis (HT). Whole blood specimens and clinical data were collected from 508 AITD patients (326 with GD and 182 with HT) and 224 age- and gender-matched healthy controls, respectively. IL-17A (rs2275913, rs8193037, rs3819025) polymorphism was determined using DNA sequencing method and IL-17F/rs763780 polymorphism was assayed by polymerase chain reaction-restriction fragment length polymorphism (PCR -RFLP). The results indicated that the frequencies of IL-17F/rs763780 genotypes in patients with GD and HT differed significantly from their controls (P = 0.013 and P = 0.005, respectively); the G allele frequencies were also significantly higher in the patient groups than the control groups (P = 0.002 and 0.001, respectively). For IL-17A/rs2275913 and rs8193037 SNP, no significant difference was observed in patients with either GD or HT compared to the control groups (P>0.05). Interestingly, for rs3819025, the frequency of A allele was lower in patients with GD than controls (P = 0.011). The frequencies of haplotype AGGG and GGGG in patients with GD and HT were significantly higher than in controls (P = 0.012, P = 0.019, P = 0.017 and P = 0.029, respectively). In conclusion, the results indicate that IL-17F/rs763780 polymorphisms may affect the susceptibility to AITD, and IL-17A/rs3819025 SNP is likely a protective factor to GD in the Chinese population.
    No preview · Article · Jul 2012 · Autoimmunity

Publication Stats

48 Citations
27.22 Total Impact Points


  • 2015
    • Shanghai Jiao Tong University
      Shanghai, Shanghai Shi, China
  • 2012-2015
    • Fudan University
      Shanghai, Shanghai Shi, China
  • 2013-2014
    • Xi'an Jiaotong University
      • Department of Endocrinology
      Ch’ang-an, Shaanxi, China