The expression of STAT3 inhibited the NF-ΚB signalling pathway and reduced inflammatory responses in mice with viral myocarditis

Li, Zhihui; Wang, Chenqiong; Mao, Yun; Cui, Jieke; Wang, Xi; Dang, Juan; Wang, Shilei

doi:10.1016/j.intimp.2021.107534

Cited by 12 publications

(4 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is released from the cytoplasm by the inhibitor protein IκBα and is moved into the nucleus. Translocated NF-κB interacts with the promoter region of the target genes, increasing the transcription of inflammatory cytokines, adhesion molecules, and chemokines [38]. In this research, we examined the mechanisms by which THMX inhibits neuroinflammation.…”

Section: Discussionmentioning

confidence: 99%

Anti-Inflammatory Activity of 1,6,7-Trihydroxy-2-(1,1-dimethyl-2-propenyl)-3-methoxyxanthone Isolated from Cudrania tricuspidata via NF-κB, MAPK, and HO-1 Signaling Pathways in Lipopolysaccharide-Stimulated RAW 264.7 and BV2 Cells

Ko,

Baek,

Liu

et al. 2023

Molecules

View full text Add to dashboard Cite

Neuroinflammation activated by microglia affects inflammatory pain development. This study aimed to explore the anti-inflammatory properties and mechanisms of 1,6,7-trihydroxy-2-(1,1-dimethyl-2-propenyl)-3-methoxyxanthone (THMX) from Cudrania tricuspidata in microglia activation-mediated inflammatory pain. In RAW 264.7 and BV2 cells, THMX has been shown to reduce lipopolysaccharide (LPS)-induced inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and pro-inflammatory mediators and cytokines, including nitric oxide (NO), prostaglandin (PG) E2, interleukin (IL)-6, and tumor necrosis factor alpha (TNF-α). THMX also decreased LPS-induced phosphorylation of mitogen-activated protein kinase (MAPK) and the activation of p65 nuclear factor kappa B (NF-κB). Interestingly, THMX also activated heme oxygenase (HO)-1 expression. These findings suggest that THMX is a promising biologically active compound against inflammation through preventing MAPKs and NF-ĸB and activating HO-1 signaling pathways.

show abstract

Section: Discussionmentioning

confidence: 99%

Anti-Inflammatory Activity of 1,6,7-Trihydroxy-2-(1,1-dimethyl-2-propenyl)-3-methoxyxanthone Isolated from Cudrania tricuspidata via NF-κB, MAPK, and HO-1 Signaling Pathways in Lipopolysaccharide-Stimulated RAW 264.7 and BV2 Cells

Ko,

Baek,

Liu

et al. 2023

Molecules

View full text Add to dashboard Cite

show abstract

“…Activation of nuclear factor kappa-B (NF-kB) increases ubiquitin/proteasome-dependent proteolysis and contributes to the dysregulation of oxidative metabolism ( 48 ). STAT3 inhibited the NF-kB signaling pathway and reduced inflammatory responses in the heart ( 49 ). This suggests that STAT3 may contribute to cardioprotection against cancer-induced cardiac cachexia.…”

Section: Discussionmentioning

confidence: 99%

The crosstalk between STAT3 and microRNA in cardiac diseases and protection

Li²,

Li³

2022

Front. Cardiovasc. Med.

View full text Add to dashboard Cite

Signal transducer and activator of transcription 3 (STAT3), an important transcription factor and signaling molecule, play an important role in cardiac disease and protection. As a transcription factor, STAT3 upregulates anti-oxidative and anti-apoptotic genes but suppresses anti-inflammatory and anti-fibrotic genes in cardiac disease and protection. As a signaling molecule, STAT3 is the downstream or upstream of other molecules for signaling transduction, also activated in cardiac disease and protection. MicroRNAs (miRNAs) are endogenous short non-coding RNAs that regulate mRNA expression at the transcriptional level and prevent protein translation. Recently, STAT3 is reported to be not only the target of miRNA but also the inhibitor or inducer of miRNA to modify the mRNA expression profiles in cardiomyocytes resulting in different effects on cardiac disease and protection. We summarize the current knowledge on STAT3 regulation of individual miRNAs and the modulation of STAT3 by miRNAs in cardiac diseases and protection.

show abstract

“…[1][2][3][4][5]102,103] Studies using CVB3 myocarditis models have indicated that activation of innate immune cells such as macrophages and dendritic cells can indirectly contribute to Th17 cell differentiation. [104,105] Th17 cells can be activated by the NF-κB inflammatory pathway [106,107] ; additionally, both IL-23 and IL-6 and the IL-6-activated signal transducer and activator of transcription 3 (STAT3) transcription factor, are considered essential for Th17 cell differentiation, which can also be directly induced by CVB3. [107] The IL-23/Th17 pathway axis is also strongly expressed in CVB3 models.…”

Section: Animal Models Of Cvb3mentioning

confidence: 99%

Role of T Cells in Viral and Immune-mediated Myocarditis

Cheng,

Baritussio,

Giordani

et al. 2024

Cardiology Discovery

View full text Add to dashboard Cite

Myocarditis is characterized by inflammatory cell infiltration into the myocardium and a high risk of deteriorating cardiac function with a heterogeneous etiology. Both viral- and myosin-induced myocarditis experimental models are used to mimic myocarditis in humans. Here, coxsackie virus B3 (CVB3)-induced and non-virus-induced myocarditis models and data obtained in clinical studies were reviewed. Experimental murine myocarditis following immunization with α-myosin together with complete Freund adjuvant represents the classical immune-mediated model. T helper 1 (Th1) and Th2 pathways and important cytokines are involved in the autoimmunity of myocarditis, and the dynamic balance between Th17 and regulatory T cell (Treg) seems to have an important role in the process of myocarditis. The purpose of this review is to summarize the existing understanding of the immunological mechanisms underlying myocarditis and exploring gaps in knowledge in both animal and human studies, since these mechanistic insights are a critical requirement for the development of novel therapeutic and vaccination strategies.

show abstract

The expression of STAT3 inhibited the NF-ΚB signalling pathway and reduced inflammatory responses in mice with viral myocarditis

Cited by 12 publications

References 24 publications

Anti-Inflammatory Activity of 1,6,7-Trihydroxy-2-(1,1-dimethyl-2-propenyl)-3-methoxyxanthone Isolated from Cudrania tricuspidata via NF-κB, MAPK, and HO-1 Signaling Pathways in Lipopolysaccharide-Stimulated RAW 264.7 and BV2 Cells

Anti-Inflammatory Activity of 1,6,7-Trihydroxy-2-(1,1-dimethyl-2-propenyl)-3-methoxyxanthone Isolated from Cudrania tricuspidata via NF-κB, MAPK, and HO-1 Signaling Pathways in Lipopolysaccharide-Stimulated RAW 264.7 and BV2 Cells

The crosstalk between STAT3 and microRNA in cardiac diseases and protection

Role of T Cells in Viral and Immune-mediated Myocarditis

Contact Info

Product

Resources

About