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4 "Tumor Necrosis Factor"
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Original Articles
TNF-α and TNF-β Polymorphisms are Associated with Susceptibility to Osteoarthritis in a Korean Population
Lin Han, Joo Hyoun Song, Jung Hwan Yoon, Yong Gyu Park, Suk Woo Lee, Yoo Jin Choi, Suk Woo Nam, Jung Young Lee, Won Sang Park
Korean J Pathol. 2012;46(1):30-37.   Published online February 23, 2012
DOI: https://doi.org/10.4132/KoreanJPathol.2012.46.1.30
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  • 49 Download
  • 28 Crossref
AbstractAbstract PDF
Background

The tumor necrosis factor (TNF) is believed to play an important role in the pathophysiology of osteoarthritis (OA). Evidence shows that genetic polymorphisms make substantial contributions to the etiology of OA.

Methods

We investigated the genotypes TNF-α and TNF-β in 301 OA patients and 291 healthy subjects as controls. We employed a polymerase chain reaction-restriction fragment length polymorphism and a polymerase chain reaction-single strand conformation polymorphism assay to identify the genotypes TNFA -G308A and TNFB +G252A, respectively.

Results

For TNFA -G308A, the percentages of genotypes GG, AG, and AA were 26.3% (79/301), 62.5% (188/301), and 11.3% (34/301) in OA patients and 88.7% (258/291), 11.3% (33/291), and 0% (0/291) in controls. For TNFB +G252A, the percentages of genotypes GG, AG, and AA were 15.3% (46/301), 41.9% (126/301), and 42.9% (129/301) in OA patients and 12% (35/291), 52.6% (153/291), and 35.4% (103/291) in controls. There were significant differences in genotypes and alleles of TNFA -308 between OA patients and controls (p<0.0001) and in alleles of TNFB +252 (p=0.0325). The risk of OA was significantly higher for carriers of the TNFA -308A allele and the TNFB +252 AA homozygote (p=0.0224).

Conclusions

The results suggest close relationships between TNFA -G308A and TNFB +G252A polymorphisms and individual susceptibility to OA in the Korean population.

Citations

Citations to this article as recorded by  
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  • Complete sequence and comparative analysis of the mitochondrial genome of the rare and endangered Clematis acerifolia, the first clematis mitogenome to provide new insights into the phylogenetic evolutionary status of the genus
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  • Relationship Between Genetic Polymorphisms of the TNF Gene and Hallux Valgus Susceptibility
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  • Functional status and severity of osteoarthritis in elderly is associated to the polymorphism of TNFA gene
    Marcos Tadeu Parron Fernandes, Karen Barros Parron Fernandes, Fernanda Freitas Anibal, Walquíria Shimoya-Bittencourt, Viviane Martins Santos, Priscila Daniele de Oliveira Perrucini, Regina Célia Poli-Frederico
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  • Association of TNF-α-308 G > A and −238G > A polymorphisms with knee osteoarthritis risk: A case-control study and meta-analysis
    Mohammad Reza Sobhan, Masoud Mahdinezhad-Yazdi, Kazem Aghili, Masoud Zare-Shehneh, Shohreh Rastegar, Jalal Sadeghizadeh-Yazdi, Hossein Neamatzadeh
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    Jie Chen, Yu Wu, Jiannong Yu, Jinming Shen
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  • Association of cytokine gene polymorphisms with osteoarthritis susceptibility
    Otilia Rogoveanu, Daniela Calina, Mihai Cucu, Florin Burada, Anca Docea, Simona Sosoi, Emilian Stefan, Mihai Ioana, Emilia Burada
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  • TNF‑α increases the expression of inflammatory factors in synovial fibroblasts by inhibiting the PI3K/AKT pathway in a rat model of monosodium iodoacetate‑induced osteoarthritis
    Hongxi Li, Shujuan Xie, Yunlong Qi, Huazhe Li, Rui Zhang, Yongyun Lian
    Experimental and Therapeutic Medicine.2018;[Epub]     CrossRef
  • The single-nucleotide polymorphism (SNP) of tumor necrosis factor α −308G/A gene is associated with early-onset primary knee osteoarthritis in an Egyptian female population
    Sahar M. Abdel Galil, Nillie Ezzeldin, Faten Fawzy, Mohamed El-Boshy
    Clinical Rheumatology.2017; 36(11): 2525.     CrossRef
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    Renhao Ze, Shangyu Wang, Mao Xie, Bo Zhang, Xin Tang, Jin Li
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  • The Role of Inflammatory and Anti-Inflammatory Cytokines in the Pathogenesis of Osteoarthritis
    Piotr Wojdasiewicz, Łukasz A. Poniatowski, Dariusz Szukiewicz
    Mediators of Inflammation.2014; 2014: 1.     CrossRef
  • Meta-analysis of tumor necrosis factor alpha -308 polymorphism and knee osteoarthritis risk
    Suotang Kou, Yaochi Wu
    BMC Musculoskeletal Disorders.2014;[Epub]     CrossRef
  • Astaxanthin reduces matrix metalloproteinase expression in human chondrocytes
    Wei-Ping Chen, Yan Xiong, Yong-Xiang Shi, Peng-Fei Hu, Jia-Peng Bao, Li-Dong Wu
    International Immunopharmacology.2014; 19(1): 174.     CrossRef
  • Variations in the TNFα gene and their interactions with the IL4R and IL10 genes in relation to hand osteoarthritis
    Satu Hämäläinen, Svetlana Solovieva, Tapio Vehmas, Päivi Leino-Arjas, Ari Hirvonen
    BMC Musculoskeletal Disorders.2014;[Epub]     CrossRef
  • Tumor necrosis factor gene polymorphisms and endometriosis in Asians: a systematic review and meta-analysis
    Jiangtao Lyu, Hua Yang, Jinghe Lang, Xianjie Tan
    Chinese Medical Journal.2014; 127(9): 1761.     CrossRef
  • Association analysis of two candidate polymorphisms in the Tumour Necrosis Factor-α gene with osteoarthritis in a Chinese population
    Bin Ji, Jixiang Shi, Xiangyu Cheng, Junjie Zhou, Qiang Zhou, Chengfu Cao, Jinhui Pang
    International Orthopaedics.2013; 37(10): 2061.     CrossRef
Immunohistochemical Study of IL-4, IL-6, and TNF Expression in Cardiac Myxoma: Emphasis on Constitutional Symptoms of the Myxoma Patients.
Min Sun Cho, Soo Yeon Cho, Mi Jung Kim, Sung Sook Kim, Jeong Wook Seo, Woon Sup Han
Korean J Pathol. 1995;29(5):563-571.
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AbstractAbstract
It is well documented that cardiac myxomas are associated with immunologic features that can simulate systemic autoimmune diseases. Recently, it was reported that cardiac myxomas produce IL-6 constitutively, which could partly explain the immunologic features observed in these patients. However, only a few investigators have studied cytokines in regards to symptoms they may cause in patients with cardiac myxoma. Also there is very little information in the literature on the immunohistochmical localization of IL-6. We performed immunobistochemical stains for IL-4, TNF, and IL-6 on paraffm embbeded tissue of cardiac myxoma tissue. A bioassay of IL-6 activity in patient's serum and in cultured cells from fresh myxoma tissue was performed to ascertain the role of these cytokines in myxomas. In this study, we demonstrated inununohistochemically that there was a local overproduction of IL-4, TNF, and IL-6 in cytoplasm of the tumor cells in about half cases. Bioassays of the serum and cultured tumor cells revealed elevated IL-6 activities. Also these findings correlate to production of patient's constitutional symptoms with statistical significance (P<0.05). In conclusion, these results are of considerable importance in understanding the role of IL-4, TNF, and IL-6 in cardiac myxoma patient with constitutional symptoms, and have an impact on strategies for diagnosis and therapy of cardiac myxoma.
Expression of Inducible Nitric Oxide Synthase and Nitric Oxide Mediated Apoptosis in Neuronal PC12 Cells after Lipopolysaccharide/Tumor Necrosis Factor-/Interferon- Treatment.
Jiyeon Kim, Jiyoung Kim, Kuseong Kang, Eunkyoung Kwak, Jiyoung Park, Taein Park, Yoonkyung Sohn
Korean J Pathol. 2002;36(4):249-256.
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  • 20 Download
AbstractAbstract PDF
BACKGROUND
Inducible nitric oxide synthase (iNOS) has been detected in a number of pathologic conditions in the central nervous system. This study was investigated the patterns of iNOS expression in the neuronal PC12 cell and the effects of nitric oxide on the apoptosis of PC12 cells.
METHODS
The stimulating agents for induction of iNOS expression in PC12 cells were bacterial lipopolysaccharide (LPS), tumor necrosis factor-alpha (TNF-), and interferon-gamma (IFN-).
RESULTS
The expression iNOS mRNA and protein in PC12 cells stimulated with LPS/TNF-/IFN- were profoundly increased. The expression of iNOS mRNA arose at 6 hours, peaked at 12 hours, and declined to 48 hours after LPS/TNF-/ IFN- treatment. iNOS protein was increased up to 24 hours in LPS/TNF-/IFN- treated PC12 cells while the expression of nNOS was unaffected. Accumulation of NO derivatives in the culture media was markedly increased at least at up to 48 hours after LPS/TNF-/IFN- treatment. The induction of iNOS expression and NO production in differentiated PC12 cells was correlated with apoptotic cell death judged by transmission electron microscopy and DNA fragmentation from the results of the Terminal deoxynucleotidyl-transferase-mediated dUDP biotin nick end-labeling (TUNEL) method. After treatment with NOS inhibitor, N-monomethylarginine (NMMA), a profound decrease in NO production by LPS/TNF-/IFN- treated PC12 cells was noted. And the LPS/TNF-/IFN- induced apoptosis was prevented by the NMMA treatment.
CONCLUSIONS
From the above results it is concluded that the expression of iNOS in differentiated PC12 cells is induced by the combined application of LPS, TNF-, and IFN-. And the apoptosis of cultured PC12 cells is mediated by iNOS-derived NO.
Expression of Tumor Necrosis Factor-alpha, Interleukin-1beta and Inducible Nitric Oxide Synthase after Stereotaxic Injection of Lipopolysaccharide in Rat Hippocampus.
Hoon Kyu Oh, Ku Seong Kang, Ji Yeon Kim, Eun Kyoung Kwak, Jung Wan Kim, Ji Young Park, Yoon Kyung Sohn
Korean J Pathol. 2004;38(3):157-164.
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AbstractAbstract PDF
BACKGROUND
Brain inducible nitric oxide synthase (iNOS) might be detectable in several pathologic conditions, and it is thought to play an important role in their pathophysiology. Tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta are believed to be essential factors of iNOS induction of the brain.
METHODS
After intrahippocampal stereotaxic injection of lipopoly-saccharide (LPS), the rat brains were removed at 6, 12 and 24 h. The rat brain tissues were examined to clarify the expression patterns of TNF-alpha, IL-1beta and iNOS.
RESULTS
The inflammatory cells which were stained with anti-TNF-alpha antibody, appeared in 6 h and increased for 24 h after LPS injection. The iNOS positive cells appeared after 12 h of LPS injection. A semiquantitative analysis of reverse transcription-polymerase chain reaction (RT-PCR) revealed that the TNF-alpha and IL-1beta mRNA arose at 1 h, peaked at 6 h and then declined until 48 h after LPS injection. The iNOS mRNA arose after 6 h, peaked at 12 h, and declined until 48 h after LPS injection.
CONCLUSIONS
We conclude that the induction of inflammatory events by intrahippocampal injection of LPS activates TNF-alpha and IL-1beta secretion, and this is followed by an induction of iNOS expression. TNF-alpha and IL-1beta seem to be related with iNOS expression in brain inflammation.

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