Wei Yin

Wuhan Children's Hospital, Wu-han-shih, Hubei, China

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Publications (9)18.79 Total impact

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    ABSTRACT: IgA vasculitis (IgAV), previously named as Henoch-Schönlein purpura, is the most common systematic vasculitis with unknown etiology. Lack of appropriate study system and/or animal model limits the understanding of its molecular pathogenesis and hinders the identification of targets for rational therapy, especially for its long-term complication, IgAV nephritis (IgAVN). In this study, we applied comparative analysis of serum proteomes to obtain an insight about disease pathogenesis. This study has utilized high sensitivity nanoscale ultra performance liquid chromatography-mass spectrometry (nanoLC-MS/MS) to investigate the alterations in serum proteomic profiles in patients with IgAV (n=6), IgAVN (n=6) and healthy subjects (n=7). The differentially expressed proteins were subjected to functional pathway analysis by PANTHER and DAVID software. We identified 107 differentially expressed proteins among three different groups, and functional analysis suggested that, in addition to earlier reported pathways, such as acute phase response, immune response, complement and blood coagulation pathways, hemostasis and Wnt signaling pathway were probably involved in pathogenesis of IgAV. A few differentially abundant proteins identified, such as C4a, serum amyloid A, angiotensinogen, and kininogen 1, were further validated by ELISA. More importantly, we found that angiotensinogen concentration is correlated with IgAVN and could be used as a potential marker for the progression of IgAV. This is the first report of analyzing the proteomic alterations in IgAV patients and the differentially proteins identified in this study may enhance understanding of the pathology of IgAV and a few of them may be used to monitor disease progression.
    PLoS ONE 06/2015; 10(6):e0130536. DOI:10.1371/journal.pone.0130536 · 3.23 Impact Factor
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    ABSTRACT: Henoch-Schönlein purpura (HSP) is the most common form of systemic vasculitis of unknown etiology. This study aimed at reviewing published studies investigating the association of genetic polymorphisms with HSP and its severity. We systematically reviewed all published data on genetic risk factors for HSP by searching MEDLINE. We also performed a meta-analysis of association studies of HLA-DRB1-01, 07, and 11, angiotensin I-converting enzyme (ACE) insertion/deletion (I/D) polymorphism. We identified 45 studies investigating polymorphisms in 39 genes in association with HSP and/or its severity. Most of these genes are involved in immunological and/or inflammatory responses or vasomotor regulation. Most results were negative. The most convincing finding is the association of HLA-DRB1*01, 07, and 11 with HSP susceptibility. The overall odds ratios (ORs) for the three loci were significant for HSP: HLA-DRB1*01 (OR = 1.805, 95 % CI 1.259-2.588, p = 0.0012); HLA-DRB1*07 (OR = 0.671, 95 % CI 0.469-0.961, p = 0.058); HLA-DRB1*11 (OR = 2.001, 95 % CI 1.50-2.67, p = 0.027). Genetic regulation of endothelial function, such as polymorphisms in genes coding rennin-angiotensin system (RAS) components, endothelial nitric oxide synthases, Inter-Cellular Adhesion Molecule 1, and vascular endothelial growth factor, could also confer effect on HSP. In addition, MEFV, whose mutations cause familial Mediterranean fever, could be an important candidate gene for HSP. Further large studies are required to investigate the association between genetic polymorphisms and HSP. Alternative approaches, such as genome-wide association study, are necessary to help to identify genetic risks for HSP.
    Rheumatology International 01/2013; 33(6). DOI:10.1007/s00296-012-2661-4 · 1.52 Impact Factor
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    ABSTRACT: Henoch-Schönlein purpura nephritis (HSPN) is the most serious long-term complication of Henoch-Schönlein purpura and aberrant galactosylation of IgA1 plays a role in its development. However, the precise role of genetic factors contributing to the abnormal IgA1 galactosylation remains unknown. In order to examine the effects of C1GALT1 gene encoding core 1 β1,3-galactosyltransferase, an important role in the β1,3 glycosylation of IgA1, on HSPN susceptibility, we conducted a case-control association genetic study in 269 HSP and 61 HSPN in China. Five tagging SNPs, SNP1(-734 C/T), SNP4(-465A/G), SNP6(-330 G/T), SNP7(-292 C/-), and SNP8(1365 G/A) in C1GALT1 were studied using single-locus and haplotype-based multilocus analysis. Our results demonstrated that 1365 G allele frequency was significantly higher in HSPN patients than in HSP patients without nephritis (0.459 vs 0.331, p = 0.0008, adjusted p' = 0.004) with an odds ratio (OR) = 1.716, 95%CI 1.151-2.560). The GG genotype of 1,365 G/A was significantly different in HSP without nephritis and HSPN (p = 0.008, adjusted p'' = 0.04). We did not observe statistically significant differences in haplotype frequencies between HSPN and HSP patients. In conclusion, our study suggested that the 1365 G/A polymorphism of the C1GALT1 gene may contribute to HSPN development.
    Pediatric Nephrology 04/2012; 27(9):1505-9. DOI:10.1007/s00467-012-2178-9 · 2.86 Impact Factor
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    ABSTRACT: Henoch-Schönlein purpura (HSP) is considered as an immune-mediated inflammatory disease. Serum amyloid A (SAA) is an acute-phase protein with proinflammatory effects. We investigated the levels of SAA in HSP patients and examined whether SAA levels are associated with organ involvement and disease severity. Seventy patients with HSP, including 35 with nephritis (HSPN) and 35 without HSPN, and 20 controls were recruited in our study. SAA levels were measured and other clinical laboratory parameters, including C-reactive protein, erythrocyte sedimentation rate, complement 3 (C3), C4, and immunoglobulin (Ig) A, were recorded. SAA levels were not found to be independently associated with renal, joint involvement, and disease severity. However, higher SAA levels were observed in HSP patients with gastrointestinal (GI) manifestations (p=0.006, p (c)=0.048). Moreover, the levels of SAA were significantly associated with duration of disease (p<0.005, p(c)<0.04). Our findings suggested that SAA was significantly associated with disease duration and GI manifestations in HSP patients.
    Inflammation 02/2012; 35(4):1251-5. DOI:10.1007/s10753-012-9435-8 · 2.21 Impact Factor
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    ABSTRACT: To assess the association of nuclear factor-kappa B (NF-κB) and complications of Kawasaki disease (KD) in Chinese children. Based on color Doppler examination results, 86 affected children in the KD group were divided into two groups: 39 cases in coronary artery lesion group (CALs subgroup) and 47 cases in non-coronary artery lesion group (Non-CALs subgroup). Infection control group consisted of 65 cases of hospitalized infected children with fever, having same age as the affected children. Healthy control group consisted of 102 cases of healthy children of the same age, visiting the hospital for physical examination. Western blot was used to detect the expression of NF-кBp65 and IкBα proteins in periphery blood mononuclear cells (PBMC); reverse transcription polymerase chain reaction (RT-PCR) was used to detect the expression of TNF-α and MCP-1 mRNA. The value of NF-kBp65 (optical density) in the PBMC cell nuclei in the KD group was significantly higher than that in the two control groups (p < 0.01). The value of NF-κBp65 in the CALs subgroup was significantly higher than that in the Non-CALs subgroup (p < 0.05). The value of NF-κBp65 inhibitor IκBα in the KD group was significantly lower than that in the infection control group and the healthy control group (p < 0.01). There was a positive correlation between the ratio nucleus NF-κBP65/ IκBα and the severity degree of CALs(r = 0.536, p < 0.05). The value of TNF-α mRNA (O.D ratio) in the KD group was significantly higher than that in the two control groups (P < 0.01), and the value of TNF-α mRNA in the CALs subgroup was significantly higher than that in the Non-CALs subgroup (P < 0.05). The value of MCP-1 mRNA in the KD group was significantly higher than that in the two control groups (P < 0.01), and the value of MCP-1 mRNA in the CALs subgroup was significantly higher than that in the Non-CALs subgroup (P < 0.05). NF-κBp65 participates in the pathogenesis of vasculitis of KD in acute stage, and may aggravate the vasculitis in KD and plays a part in the formation of CALs.
    The Indian Journal of Pediatrics 06/2011; 78(11):1378-82. DOI:10.1007/s12098-011-0478-x · 0.87 Impact Factor
  • X He · S Kang · Z Liu · W Yin · Y Ding
    Scandinavian journal of rheumatology 03/2011; 40(3):238-9. DOI:10.3109/03009742.2011.553737 · 2.53 Impact Factor
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    ABSTRACT: Henoch-Schönlein purpura (HSP) is an immune complex-mediated systemic vasculitis. Its genetic etiology remains unknown. CD18, the subunit of integrin beta2 in leukocytes, has essential roles in the expression and function of ITGB2, mediating immune responses. CD18 has been proved to be associated with some systemic vasculitides, such as microscopic polyangiitis and Churg-Strauss syndrome. We aimed to assess the influence of CD18 AvaII polymorphism (rs235326, C->T) in the incidence of HSP and determine its possible implication in severe systemic complications by studying 73 patients with HSP and 156 controls in China. Our results showed that AvaII polymorphism was not associated with HSP susceptibility (odd ratio (OR)=0.48, 95% confidence interval (CI)=0.53-1.39, p=0.63) or with HSP nephritic syndrome (OR=0.88, 95%CI=0.35-2.06, p=0.90). Moreover, we did not observe any significant association between serum parameters, such as CRP, IgA, IgE, C3 and C4, and HSP severity. In conclusion, our results suggested that CD18 AvaII is not associated with HSP susceptibility and its clinical outcomes.
    Clinical and experimental rheumatology 12/2010; 29(1 Suppl 64):S117-20. · 2.72 Impact Factor
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    ABSTRACT: Henoch-Schönlein purpura (HSP) is a multifactorial inflammatory disease whose pathogenesis remains unknown. Pyrin encoded by the MEFV gene (NM_000243; OMIM 608107) is an important active member of the inflammasome and has been shown to affect the expression of many of the genes involved in immune and inflammatory responses. The aim of our study was to elucidate the possible roles of MEFV genetic variants on the susceptibility to HSP and its clinical outcomes in 78 patients with HSP and 189 controls in China. A significant association was found between the E148Q polymorphism (G->C) and HSP susceptibility (odds ratio 2.76, 95% confidence interval 1.76-4.34, P=0.0001). The C allele of E148Q was associated with joint involvement (P=0.014) but not with HSP nephritis (P=0.1). The clinical score was higher in subjects with the CC genotype than in those with the CG or GG genotype (4.13+/-3.53 vs. 1.94+/-1.70, respectively; P=0.011). P369S was not associated with HSP or other phenotypes. M694V and M680I were absent in our patients. Our results suggest that MEFV E148Q could be a contributory genetic factor to HSP and HSP-related joint syndromes.
    Pediatric Nephrology 10/2010; 25(10):2077-82. DOI:10.1007/s00467-010-1582-2 · 2.86 Impact Factor
  • Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics 08/2010; 12(8):675-6.