TRIM59 expression is regulated by Sp1 and Nrf1 in LPS-activated macrophages through JNK signaling pathway

An, Yanying; Ni, Yuqi; Xu, Zhihao; Shi, Shuizhen; He, Jiashu; Liu, Yu; Deng, Ke-Yu; Fu, Mingui; Jiang, Meixiu; Xin, Hong‐Bo

doi:10.1016/j.cellsig.2019.109522

Cited by 24 publications

(33 citation statements)

References 53 publications

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“…Trim59 participates in many pathological processes, such as inflammation, cytotoxicity and tumorigenesis, as a member of the TRIM protein superfamily. Trim59 expression is inhibited by LPS and TLR3 ligands in macrophages ( 23 , 24 ). Furthermore, Trim59 interacts with evolutionarily conserved signaling intermediates in Toll pathways and negatively regulates NF-κB- and IRF-3/7-mediated signaling pathways ( 25 ).…”

Section: Resultsmentioning

confidence: 99%

METTL3-Mediated N6-Methyladenosine Modification of Trim59 mRNA Protects Against Sepsis-Induced Acute Respiratory Distress Syndrome

Chen

Zhu

et al. 2022

Front. Immunol.

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N6-methyladenosine (m6A) RNA modification is a fundamental determinant of mRNA metabolism in eukaryotic cells and is involved in numerous physiological and pathological processes. However, the specific role of m6A modification in sepsis-induced acute respiratory distress syndrome(ARDS) remains unknown. Here, we show that the levels of m6A RNA were significantly decreased in septic lungs and that METTL3 was the main regulator involved in the absence of m6A RNA modification. Pulmonary endothelial barrier damage is a critical process in the pathogenesis of acute lung injury during sepsis. METTL3 regulated endothelial barrier dysfunction and inflammatory responses in sepsis-induced ARDS in vivo and in vitro. Furthermore, we identified tripartite motif-containing (Trim)59 as a key m6A effector and Trim59 deficiency exacerbated lung injury. Mechanistically, METTL3 inhibited endothelial injury in sepsis-induced ARDS through Trim59-associated NF-κB inactivation. Our findings revealed novel insights into epitranscriptional mechanisms in sepsis-induced ARDS via m6A modifications, which has important application value in the diagnosis, prognosis, and molecular-targeted therapy of sepsis-associated lung injury.

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Section: Resultsmentioning

confidence: 99%

METTL3-Mediated N6-Methyladenosine Modification of Trim59 mRNA Protects Against Sepsis-Induced Acute Respiratory Distress Syndrome

Chen

Zhu

et al. 2022

Front. Immunol.

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“…Previous literature revealed that SP1 could bind to the promoter region of HDAC4 to promote its transcriptional activation, and meanwhile, HDAC4 inhibited the occurrence of sepsis [ 9 , 11 ]. Therefore, we chose HDAC4 as the SP1 downstream target for the following experiment.…”

Section: Resultsmentioning

confidence: 99%

“…Specificity protein-1 (SP1) belongs to the member of the SP family of transcription factors [ 7 ] and is implicated in inflammation and genomic instability as well as epigenetic silencing [ 8 ]. In lipopolysaccharide (LPS)-activated macrophages, SP1 can directly bind to the proximal promoter of TRIM59 gene which may serve as a potential therapeutic target for inflammatory diseases [ 9 ]. A recent work revealed that SP1 binds to the histone deacetylase 4 (HDAC4) gene promoter sequence and induces the consequent upregulation of HDAC4 mRNA and protein expressions in SH-SY5Y neuroblastoma cells [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

SP1 Promotes HDAC4 Expression and Inhibits HMGB1 Expression to Reduce Intestinal Barrier Dysfunction, Oxidative Stress, and Inflammatory Response after Sepsis

Liu

Wang

et al. 2022

J Innate Immun

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As a serious and elusive syndrome caused by infection, sepsis causes a high rate of mortality around the world. Our investigation aims at exploring the role and possible mechanism of specificity protein-1 (SP1) in the development of sepsis. A mouse model of sepsis was established by cecal ligation perforation, and a cellular model was stimulated by lipopolysaccharide (LPS), followed by determination of the SP1 expression. It was determined that SP1 was poorly expressed in the intestinal tissues of septic mice and LPS-treated cells. Next, we examined the interactions among SP1, histone deacetylase 4 (HDAC4), and high mobility group box 1 (HMGB1) and found that SP1 bound to the HDAC4 promoter to upregulate its expression, thereby promoting the deacetylation of HMGB1. Meanwhile, gain- or loss-of-function approaches were applied to evaluate the intestinal barrier dysfunction, oxidative stress, and inflammatory response. Overexpression of SP1 or underexpression of HMGB1 was observed to reduce intestinal barrier dysfunction, oxidative stress, and inflammatory injury. Collectively, these experimental data provide evidence reporting that SP1 could promote the HDAC4-mediated HMGB1 deacetylation to reduce intestinal barrier dysfunction, oxidative stress, and inflammatory response induced by sepsis, providing a novel therapeutic target for sepsis prevention and treatment.

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“…Macrophages are responsible for the release of proinflammatory cytokines such as IL-1, TNF-α, IL-6. Macrophages play an important role in immune response, and abnormal activation of macrophages frequently leads to inflammatory and immune diseases (13,14). Crinum latifolium belongs to Amaryllidacea and is generally used in traditional medicine in different regions around the world.…”

Section: Discussionmentioning

confidence: 99%

“…The activated macrophages play a significant role in immune response, and abnormal macrophage activation frequently leads to immune and inflammatory diseases. However, the mechanisms of macrophage activation are not completely understandable (13,14). The LPS induced macrophage activation plays an important role in many chronic inflammations.…”

Section: Introductionmentioning

confidence: 99%

Crinum latifolium extract inhibits lipopolysaccharide-induced inflammation in human macrophages

Köktürk

Çetinkol

Cırrık

2022

Revista Romana De Medicina De Laborator

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Introduction: Crinum latifolium is a natural plant showing the anti-inflammatory effects. We aimed to evaluate the effects of Crinum latifolium extract on proinflammatory cytokine production and maturation of early and late endosomes in the lipopolysaccharide (LPS)-induced human macrophages at light microscopic and biochemical levels. Material and Methods: The effects of Crinum latifolium extract in human macrophages stimulated with LPS was evaluated to optic densities of the lysosome-associated membrane protein-1 (LAMP-1) and early endo-some antigen 1 (EEA1) by immunohistochemistry staining and to level of the proinflammatory cytokine interleukin (IL)-6 by enzyme-linked immunosorbent assay (ELISA). Results: Crinum latifolium group exhibited a significant decreased in the levels of IL-6 in the supernatant as compared to the LPS group for 2 and 72 hours (p<0.0001). Crinum latifolium group exhibited a significant increased in the optic density of the EEA1 and LAMP-1 in coverslips as compared to the control and lipopolysaccharide groups after 2 and 72 hours (p<0.0001). Conclusions: Crinum latifolium may a therapeutic plant in the inflammatory diseases, such as sepsis, through anti-inflammatory effects, such as decrease in production of the proinflammatory cytokine and increase in maturations of the early and late endosomes in macrophages.

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TRIM59 expression is regulated by Sp1 and Nrf1 in LPS-activated macrophages through JNK signaling pathway

Cited by 24 publications

References 53 publications

METTL3-Mediated N6-Methyladenosine Modification of Trim59 mRNA Protects Against Sepsis-Induced Acute Respiratory Distress Syndrome

METTL3-Mediated N6-Methyladenosine Modification of Trim59 mRNA Protects Against Sepsis-Induced Acute Respiratory Distress Syndrome

SP1 Promotes HDAC4 Expression and Inhibits HMGB1 Expression to Reduce Intestinal Barrier Dysfunction, Oxidative Stress, and Inflammatory Response after Sepsis

Crinum latifolium extract inhibits lipopolysaccharide-induced inflammation in human macrophages

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