TRIM59 expression is regulated by Sp1 and Nrf1 in LPS-activated macrophages through JNK signaling pathway
| Autor: | Yu Liu, Hongbo Xin, Yuqi Ni, Zhihao Xu, Ke-Yu Deng, Mingui Fu, Jiashu He, Shui-Zhen Shi, Yanying An, Meixiu Jiang |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Lipopolysaccharides Male Transcription Genetic MAP Kinase Signaling System Sp1 Transcription Factor NF-E2-Related Factor 1 Inflammation medicine.disease_cause Models Biological Article Tripartite Motif Proteins 03 medical and health sciences Mice 0302 clinical medicine In vivo medicine Macrophage Animals Humans NRF1 Cytotoxicity Promoter Regions Genetic Gene Base Sequence Chemistry Macrophages Intracellular Signaling Peptides and Proteins Cell Biology Macrophage Activation Atherosclerosis In vitro Cell biology Mice Inbred C57BL Protein Transport 030104 developmental biology RAW 264.7 Cells Gene Expression Regulation 030220 oncology & carcinogenesis Disease Progression medicine.symptom Carcinogenesis |
| Zdroj: | Cell Signal |
| Popis: | Activated macrophages play an important role in many inflammatory diseases including septic shock and atherosclerosis. TRIM59 has been showed to participate in many pathological processes, such as inflammation, cytotoxicity and tumorigenesis. However, the molecular mechanisms controlling its expression in activated macrophages are not fully understood. Here we report that TRIM59 expression is regulated by Sp1 and Nrf1 in LPS-activated macrophages. TRIM59 is highly expressed in macrophages, and markedly decreased by LPS stimuli in vivo and in vitro. TRIM59 promoter activity is also significantly suppressed by LPS and further analysis demonstrated that Sp1 and Nrf1 directly bound to the proximal promoter of TRIM59 gene. LPS treatment significantly decreased Sp1 expression, nuclear translocation and reduced its binding to the promoter, whereas increased Nrf1 expression, nuclear translocation and enhanced its binding to the promoter. Moreover, LPS-decreased TRIM59 expression was reversed by JNK inhibitor. Finally, TRIM59 level is significantly decreased during atherosclerosis progression. Taken together, our results demonstrated that TRIM59 expression was precisely regulated by Sp1 and Nrf1 in LPS-activated macrophages, which may be dependent on the activation of JNK signaling pathway and TRIM59 may be a potential therapeutic target for inflammatory diseases such as atherosclerosis. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|