Lifang Tian

Xi'an Jiaotong University, Xi’an, Shaanxi Sheng, China

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Publications (7)24.35 Total impact

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    ABSTRACT: T-2 toxin (T-2), one of the most important and toxic trichothecene mycotoxins, can cause many medical problems, such as diarrhea, nervous disorders, immunodepression and death, and is also believed as an etiological factor of Kashin-Beck disease, an endemic osteochondropathy prevailing in North China. However, the molecular mechanisms underlying T-2 effects on tissue damage remain elusive. We differentiated ATDC5 chondrogenic cells into hypertrophic chondrocytes, and found that T-2 reduced the expression of anabolic genes, and increased the expression of catabolic genes. To uncover the mechanism that T-2 influenced metabolic homeostasis of hypertrophic chondrocytes, we observed that T-2 increased the production of reactive oxygen species (ROS) and the degradation of IκB-α, and up-regulated the expression of hypoxia-induced factor-2α (HIF-2α). Bay11-7085 (an inhibitor of NF-κB pathway) inhibited the up-regulation of HIF-2α, and N-acetyl-l-cysteine (a ROS scavenger) inhibited both the decrease of IκB-α and the up-regulation of HIF-2α. Our results demonstrate that ROS-NF-κB-HIF-2α pathway participates in the effects of T-2 on hypertrophic chondrocytes, and HIF-2α plays an important role as a key mediator in this process.
    Toxicology in Vitro 07/2012; 26(7):1106-13. · 2.65 Impact Factor
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    ABSTRACT: MicroRNAs (miRNAs) have been implicated in regulating diverse cellular pathways and involved in development and inflammation. This study aimed to examine six miRNAs expression during the cartilage development and identify the key miRNA which is associated with chondrogenesis. The expression of six miRNAs in cartilage tissue during development was screened by real-time quantitative polymerase chain reaction (RT-qPCR). Rat models of bone matrix gelatin induced endochondral ossification, collagen-induced arthritis and pristane-induced arthritis were established to examine whether miR-337 is involved in chondrogenesis. Furthermore, the regulation of transforming growth factor-b type II receptor (TGFBR2) expression by miR-337 was determined with the luciferase reporter gene assay and Western blot. The expression of some specific genes relevant to cartilage tissue was tested by RT-qPCR after miR-337 mimic or inhibitor transfection. MiR-337 expression was significantly down-regulated and almost disappeared in the maturation phases of endochondral ossification. The results of histology and RT-qPCR from three rat models showed that miR-337 is directly bound up with chondrogenesis. Furthermore, the results from the luciferase reporter gene assay and Western blot indicated that miR-337 regulated TGFBR2 expression. Our study also found that the enhancement of miR-337 may modulate the expression of cartilage-specific genes such as AGC1 in C-28/I2 chondrocytes. We proved that miRNA-337 is associated with chondrogenesis through regulating TGFBR2 expression, and miRNA-337 can also influence cartilage-specific gene expression in chondrocytes. These findings may provide an important clue for further research in the arthritis pathogenesis and suggest a new remedy for arthritis treatment.
    Osteoarthritis and Cartilage 03/2012; 20(6):593-602. · 4.26 Impact Factor
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    ABSTRACT: Recently, two genome scan meta-analysis studies have found strong evidence for the association of loci on chromosome 8p with schizophrenia. The early growth response 3 (EGR3) gene located in chromosome 8p21.3 was also found to be involved in the etiology of schizophrenia. However, subsequent studies failed to replicate this finding. To investigate the genetic role of EGR3 in Chinese patients, we genotyped four SNPs (average interval ∼2.3 kb) in the chromosome region of EGR3 in 470 Chinese schizophrenia patients and 480 healthy control subjects. The SNP rs35201266 (located in intron 1 of EGR3) showed significant differences between cases and controls in both genotype frequency distribution (P = 0.016) and allele frequency distribution (P = 0.009). Analysis of the haplotype rs35201266-rs3750192 provided significant evidence for association with schizophrenia (P = 0.0012); a significant difference was found for the common haplotype AG (P = 0.0005). Furthermore, significant associations were also found in several other two-, and three-SNP tests of haplotype analyses. The meta-analysis revealed a statistically significant association between rs35201266 and schizophrenia (P = 0.0001). In summary, our study supports the association of EGR3 with schizophrenia in our Han Chinese sample, and further functional exploration of the EGR3 gene will contribute to the molecular basis for the complex network underlying schizophrenia pathogenesis.
    PLoS ONE 01/2012; 7(1):e30237. · 3.73 Impact Factor
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    ABSTRACT: Primary OA and Kashin-Beck disease (KBD) show similar pathological changes in articular cartilage. The objective was to screen differentially expressed genes between OA and normal cartilage, confirm the candidate gene expression among OA, KBD and normal cartilage, and then clarify its role in vitro. Differentially expressed genes in OA cartilage were screened by suppression subtractive hybridization (SSH) and verified by real-time quantitative PCR (Q-PCR) analysis. Heparan sulphate 6-O-sulphotransferase 2 (HS6ST2) expression was identified by Q-PCR and immunohistochemistry. After suppressing HS6ST2 by RNA interference in C28/I2 human chondrocyte line, the effects were analysed through determining the cell viability by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), the aggrecan contents by toluidine blue staining and the mRNA expression levels of SRY-type high mobility group box 9 (SOX9), AGC1, MMP3, a disintegrin and metalloproteinase domain with thrombospondin motifs 4 (ADAMTS4) and ADAMTS5 by Q-PCR. HS6ST2 in the reverse subtraction library was identified as a down-regulated gene in OA and KBD at both mRNA and protein levels. The percentage of safranion O staining area was correlated positively with the percentage of HS6ST2-positive chondrocytes in OA and KBD cartilage. After HS6ST2-specific short interfering RNA (siRNA) transfection to C28/I2 cells, the cell viability was inhibited significantly, and the mRNA expression levels of SOX9 and AGC1 were reduced markedly, while MMP3 expression was increased significantly. CONCLUSION; HS6ST2 down-regulation was identified in both OA and KBD cartilage. The findings first suggest that HS6ST2 may participate in the pathogenesis of OA and KBD by influencing aggrecan metabolism.
    Rheumatology (Oxford, England) 12/2011; 50(12):2176-86. · 4.24 Impact Factor
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    ABSTRACT: Expression profiles of microRNAs (miRNAs) can shape the repertoire of proteins expressed in development, differentiation and diseases. This study aimed to identify miRNA profile of articular cartilage at different developmental stages in rats. Three small RNA libraries were constructed from the femoral head cartilage of Sprague-Dawley (SD) rats at postnatal day 0, day 21 and day 42 and sequenced by a deep sequencing approach. Then a bioinformatics approach was employed to distinguish genuine miRNAs from small RNAs represented in the mass sequencing data. The expression of indicated miRNAs was determined by stem-loop RT-qPCR to valuate the consistency with Solexa sequencing. Two hundred and fifty-eight of 310 known miRNA and miRNA* genes were organized into 91 compact clusters. Two hundred and forty-six miRNAs were detected in all three small RNA libraries of rat articular cartilage. Forty-six, fifty-two and fifty-six miRNA* genes were identified from three small RNA libraries, respectively, and 86 novel miRNA candidate genes were found simultaneously. In addition, 23 known miRNAs were up-regulated (fold change ≥ 4); six were down-regulated (fold change ≤ -4) during articular cartilage development. The predicted targets of differentially expressed miRNAs were locally secreted factors and transcription factors that regulate proliferation and differentiation of chondrocytes. The same expression tendency of indicated miRNAs during articular cartilage development stages was observed by using Solexa sequencing and stem-loop RT-qPCR. Our study provided a unique opportunity to decipher how the elaboration of the miRNA repertoire contributes to the development process of articular cartilage.
    Osteoarthritis and Cartilage 07/2011; 19(10):1237-45. · 4.26 Impact Factor
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    ABSTRACT: To examine plasma levels of arthritis-related autoantibodies and inflammatory factors in Kashin-Beck disease (KBD) patients compared with rheumatoid arthritis (RA) patients, osteoarthritis (OA) patients, and healthy controls, the plasma levels of autoantibodies to types II, IX, and XI collagen and cyclic citrullinated peptide (CCP) and immunoglobulin (Ig)-G and IgM rheumatoid factors (IgG-RF and IgM-RF) from 45 KBD patients, 39 RA patients, 46 OA patients, and 30 healthy controls were determined by enzyme-linked immunosorbent assay. The plasma concentrations of nitric oxide (NO) and tumor necrosis factor-α (TNF-α) were measured using the Griess method and bioassay, respectively. Statistical analysis was performed using one-way analysis of variance followed by the least significant difference t test for differences among groups. Results indicated that the plasma levels of collagen IX antibodies, IgG-RF, and NO significantly increased in KBD patients compared with patients with RA and OA and the control group. The levels of collagen XI antibodies, CCP antibodies, and IgM-RF but not collagen II antibodies and TNF-α were significantly increased in the plasma of the KBD group compared with that of the control group. We conclude that autoimmunity and inflammation may be involved in the pathogenesis of KBD, in particular in the advanced stage.
    Human immunology 06/2011; 72(10):812-6. · 2.55 Impact Factor
  • W Hou, L Meng, L Tian, W Zhu, C Jiang, S Lu
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    ABSTRACT: Both collagen-induced arthritis (CIA) and pristane-induced arthritis (PIA) are commonly used rat models of rheumatoid arthritis (RA). The aim of this study was systematically to compare the differences between CIA and PIA in Dark Agouti (DA) rats. The CIA was induced by immunising DA rats intradermally with collagen type (C) and PIA was induced by injecting subcutaneously with pristane. The arthritis was evaluated macroscopically and microscopically. Nitric oxide (NO) level of plasma was determined by Griess reaction method. Plasma autoimmune antibodies, including C specific IgG antibody (anti-C IgG), cyclic citrullinated peptide specific IgG antibody (anti-CCP IgG), IgM and IgG rheumatoid factors (IgM RF and IgG RF), were detected by the enzyme-linked immunosorbent assay. The onset of PIA rats was earlier than that of CIA rats. The involved sites of PIA rats were mostly wrist/ankle and metacarpophalangeal/metatarsophalangeal (MCP/MTP) joints while those of CIA rats were primarily distal interphalangeal (DIP) joints. NO level of plasma was increased in PIA rats, as anti-C IgG, anti-CCP IgG, IgM RF and IgG RF levels of plasma were increased in CIA rats. The kidney hyaline casts were more frequent in CIA rats than in control rats, with 9/12 in PIA group, 8/8 in CIA, and 4/8 in control, respectively. PIA mainly affected wrist/ankle joints and MCP/MTP joints, had more severe inflammation and hardly involved other organs; while CIA mostly influenced DIP joints, had more autoimmune antibodies in plasma, and always showed hyaline casts in kidney. These findings will be useful to select the animal model of RA.
    Clinical and experimental rheumatology 01/2010; 28(4):532-8. · 2.66 Impact Factor