Genetically Determined TNF-α Secretion Influences the Development of Dermatomyositis and Systemic Lupus Erythematosus

Dourmishev, Lyubomir; Hristova, Maria; Kamenarska, Zornitsa; Savov, Alexey; Vinkov, Anton; Kaneva, Radka; Mitev, Vanio

doi:10.1515/folmed-2017-0084

Cited by 4 publications

(2 citation statements)

References 16 publications

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“…Most polymorphisms in these genes associated with PTB were also found in mentioned pathologies. The most commonly found polymorphism is TNFα rs1800629, which is also associated with SLE, 128 IBD, 129 PD, 130 AR, 131 and IBS 132 . Other variants were found in more than one disease, namely, the IL1β rs16944 with UC 133 and AR, 131 the IL1RN rs2234663 with UC 129 and PD, 134 the IL6 rs1800795 with IBD 135 and IBS, 132 the TLR4 rs4986790 with IBD 136 and PD, 137 and finally, the TIMP2 rs8179090 with SLE 138 and PD 139 …”

Section: Autoimmune and Inflammatory Diseases Related To Ptbmentioning

confidence: 99%

Inflammatory factors, genetic variants, and predisposition for preterm birth

et al. 2021

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Preterm birth is a major clinical and public health challenge, with a prevalence of 11% worldwide. It is the leading cause of death in children younger than 5 years old and represents 70% of neonatal deaths and 75% of neonatal morbidity. Despite the clinical and public health significance, this condition's etiology is still unclear, and most of the cases are spontaneous. There are several known preterm birth risk factors, including inflammatory diseases and the genetic background, although the underlying molecular mechanisms are far from understood. The present review highlights the research advances on the association between inflammatory‐related genes and the increased risk for preterm delivery. The most associated genetic variants are the TNFα rs1800629, the IL1α rs17561, and the IL1RN rs2234663. Moreover, many of the genes discussed in this review are also implicated in pathologies involving inflammatory or autoimmune systems, such as periodontal disease, bowel inflammatory disease, and autoimmune rheumatic diseases. This review presents evidence suggesting a common genetic background to preterm birth, autoimmune and inflammatory diseases susceptibility.

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Section: Autoimmune and Inflammatory Diseases Related To Ptbmentioning

confidence: 99%

Inflammatory factors, genetic variants, and predisposition for preterm birth

et al. 2021

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“…DM is a systemic inflammatory condition characterized by cutaneous and muscle findings, in addition to the potential involvement of other organ systems. Imbalance of cytokines is determined to play a crucial role in the pathogenesis of DM (Dourmishev et al, 2018). TNF‐α as one of the intensely studied proinflammatory factors is characterized to influence the development of DM.…”

Section: Discussionmentioning

confidence: 99%

Role of DNA methylation on human CTSG in dermatomyositic myoideum

Peng

Sun

Liang

2020

Cell Biology International

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Dermatomyositis (DM) is a multifactorial chronic autoimmune disorder with characteristic skin and muscle pathological changes and involvement of other organ systems. Cathepsin G (CTSG) contributes to the risk of developing DM, which is likely to be associated with inflammatory cytokines. Differential DNA methylation on CTSG has been determined to be implicated in DM in vivo. However, the underlying mechanism of this epigenetic regulation on CTST in DM is poorly explored. In this study, we investigated DNA methylation signature on CTSG at single‐nucleotide resolution in quadriceps femoris of six DM patients and paracancerous muscles of three patients with rhabdomyosarcoma on inner thigh using pyrosequencing and observed that the overall DNA methylation level of CTSG was increased in DM compared with control, in which CpG loci at third and fourth exons but not promoter contributed to the significant hypermethylation. Furthermore, we observed that transcription and DNA methylation of CTSG were both declined in DNMT3a knockdown compared with DNMT1 and DNMT3b knockdown in human skeletal muscle SJCRH30 and A‐204 cell lines exposed to tumor necrosis factor‐α. Furthermore, Bortezomib (NF‐κB inhibitor) and Brevilin A (JAK/STAT inhibitor) were employed to treat SJCRH30 and A‐204 cells, respectively, and we observed that CTSG was hypomethylated and silenced after Bortezomib treatment compared with untreatment and Brevilin A. Finally, chromatin immunoprecipitation‐quantitative polymerase chain reaction indicated that DNMT3a could bind to the coding regions of CTSG and the interaction was dependent on NF‐κB activity. Taken together, our results determined a novel regulatory mechanism of DNA methylation on CTSG in DM.

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