Meta-analysis of tumor necrosis factor alpha -308 polymorphism and knee osteoarthritis risk

Kou, Suo-Tang; Wu, Ya‐Fen

doi:10.1186/1471-2474-15-373

Cited by 20 publications

(21 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, the presence of a variety of pain‐related molecules, including TNF, has previously been demonstrated in the subchondral bone of patients with knee OA . TNF has been proposed as a genetic risk factor in knee OA , and RNA interference–induced silencing of TNF has been demonstrated as a therapeutic in a leporine model . However, the results of human trials with TNF monoclonal antibodies in the treatment of human OA have been mixed .…”

Section: Discussionmentioning

confidence: 99%

Genome‐Wide DNA Methylation Study Identifies Significant Epigenomic Changes in Osteoarthritic Subchondral Bone and Similarity to Overlying Cartilage

Jeffries

Donica

Baker

et al. 2016

Arthritis & Rheumatology

View full text Add to dashboard Cite

Objective To perform a genome-wide DNA methylation study to identify differential DNA methylation patterns in subchondral bone underlying eroded and intact cartilage from patients with hip osteoarthritis (OA) and to compare these with DNA methylation patterns in overlying cartilage. Methods Genome-wide DNA methylation profiling using Illumina HumanMethylation 450 arrays was performed on eroded and intact cartilage and subchondral bone from within the same joint of 12 patients undergoing hip arthroplasty. Genes with differentially methylated CpG sites were analyzed to identify shared pathways, upstream regulators, and overrepresented gene ontologies, and these patterns were compared with those of the overlying cartilage. Histopathology was graded by modified Mankin score and assessed for correlation with DNA methylation. Results We identified 7,316 differentially methylated CpG sites in subchondral bone underlying eroded cartilage, most of which (~75%) were hypomethylated, and 1,397 sites in overlying eroded cartilage, 126 of which were shared. Samples clustered into 3 groups with distinct histopathologic scores. We observed differential DNA methylation of genes including the RNA interference–processing gene AGO2, the growth factor TGFB3, the OA suppressor NFATC1, and the epigenetic effector HDAC4. Among known susceptibility genes in OA, 32 were differentially methylated in subchondral bone, 8 were differentially methylated in cartilage, and 5 were shared. Upstream regulator analysis using differentially methylated genes in OA subchondral bone showed a strong transforming growth factor β1 signature (P = 1 × 10−40) and a tumor necrosis factor family signature (P = 3.2 × 10−28), among others. Conclusion Our data suggest the presence of an epigenetic phenotype associated with eroded OA subchondral bone that is similar to that of overlying eroded OA cartilage.

show abstract

Section: Discussionmentioning

confidence: 99%

Genome‐Wide DNA Methylation Study Identifies Significant Epigenomic Changes in Osteoarthritic Subchondral Bone and Similarity to Overlying Cartilage

Jeffries

Donica

Baker

et al. 2016

Arthritis & Rheumatology

View full text Add to dashboard Cite

show abstract

“…(*P<0.001 compared to untreated control; #P<0.001 compared to TNF-α treated group) Discussion TNF-α is a pro-inflammatory cytokine in many inflammatory disorders including OA. TNF-α is activated by synoviocytes and chondrocytes, and it plays a critical role in the pathogenesis of OA (Kou and Wu 2014). As a matter of fact, the increased amounts of TNF-α were found in chondrocytes and synovial cells of OA patients (Tetta et al 1990) and high concentration of TNF-α was also found in human OA cartilage (Shinmei et al 1990).…”

Section: Resultsmentioning

confidence: 96%

Inhibitory effects of EGb761 on the expression of matrix metalloproteinases (MMPs) and cartilage matrix destruction

Wang

Zhao

Tang

2015

Cell Stress and Chaperones

View full text Add to dashboard Cite

Cytokines such as tumor necrosis factor alpha (TNF-α)-induced expression of matrix metalloproteinase (MMP) play a pivotal role in the destruction of articular cartilage in patients who are suffering from osteoarthritis (OA). Collagen type II, the basis for articular cartilage, can be degraded by MMP-1, MMP-3, and 13. EGb761, the standardized extract of Ginkgo biloba produced by Dr. Willar Schwabe Pharmaceuticals, has shown its anti-inflammatory capacity. This study aimed to determine a mechanism whereby EGb761 may inhibit cartilage degradation. Our results indicated that pretreatment with EGb761 abolishes MMP-1, MMP-3, and MMP-13 gene expression and protein expression induced by TNF-α in human chondrocyte monolayer. In addition, the reduction of the tissue inhibitor of metalloproteinase-1(TIMP-1) and metalloproteinase-2 gene expression induced by TNF-α was rescued by pretreatment with EGb761. Importantly, TNF-α-induced degradation of collagen type II was ameliorated by EGb761 in a dose-dependent manner. Mechanistically, our results indicated that EGb761 treatment attenuated TNF-α-induced NF-κB activation. These actions of EGb761 suggest a mechanism by which EGb761 may act to prevent cartilage breakdown in arthritis.

show abstract

“…It has been observed that these variants are strongly associated with possibility to develop knee OA 27,33 . As per high level of expression of TNF-α with -308A allele and low expression of -308G allele, meta-analysis concluded that AA and AG genotypes influence the rate of risk of OA, whereas individuals with GG genotype might have lesser impact on developing of OA 19 . Among other variants of TNF-α, the minor allele of the "-308" locus is affecting the TNF-α protein expression under various stimuli 36 .…”

Section: Gene Variants Of Tnf-α In Osteoarthritismentioning

confidence: 99%

Association of Cytokine TNF-? in Development of Osteoarthritis: A Comprehensive Study

Kumar

Ali

Singh

et al. 2018

Journal of Ecophysiology and Occupational Health

View full text Add to dashboard Cite

Osteo-Arthritis (OA) is a disease of joints affecting the normal functions of joint and causes physical disability. Many factors are responsible for development of osteoarthritis including over age, obesity, gender, drug abuse, over load on joints and genetic factors. OA causes health problems and impairs the quality of life with increased economic burden across the world. Apart from the pro-inflammatory role of cytokine Interleukin-1 (IL-1) in osteoarthritis, Tumor necrosis factor-alpha (TNF-α) is also involved in the progression of osteoarthritis. Members of TNF family are secreted from lymphocytes and natural killer cells but in OA patients it is also secreted from chondrocyte cells to influence the catabolic processes in Extra Cellular Matrix (ECM) by inducing the activity of matrix metaloproteinases (MMPs). In promoter region, most of the Single nucleotide polymorphisms (SNPs) of TNF-α located on -863, -857, -308, and -238. These SNPs are involved in various diseases including OA, rheumatoid Arthritis, systemic lupus erythematosus etc. Significance association of SNP -G308A of the TNF-α gene in OA has been observed in various studies. Aim of this mini review is to conclude the fundamental roles of TNF-α cytokine in patients with OA.

show abstract

Meta-analysis of tumor necrosis factor alpha -308 polymorphism and knee osteoarthritis risk

Cited by 20 publications

References 29 publications

Genome‐Wide DNA Methylation Study Identifies Significant Epigenomic Changes in Osteoarthritic Subchondral Bone and Similarity to Overlying Cartilage

Genome‐Wide DNA Methylation Study Identifies Significant Epigenomic Changes in Osteoarthritic Subchondral Bone and Similarity to Overlying Cartilage

Inhibitory effects of EGb761 on the expression of matrix metalloproteinases (MMPs) and cartilage matrix destruction

Association of Cytokine TNF-? in Development of Osteoarthritis: A Comprehensive Study

Contact Info

Product

Resources

About