MiR-146a Regulates Inflammatory Infiltration by Macrophages in Polymyositis/Dermatomyositis by Targeting TRAF6 and Affecting IL-17/ICAM-1 Pathway

Yin, Yong; Li, Fēi; Shi, Jing; Li, Songlin; Cai, Jingjing; Jiang, Youyu

doi:10.1159/000452563

Cited by 37 publications

(32 citation statements)

References 40 publications

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“…This contradicts another study demonstrating increased muscle tissue IL-17 production in DM (11). Inclusion of probable patients with DM and longer average DM duration in the previous study might be potential reasons for this discrepancy.…”

Section: Correlations Between Cytokine Expression Levels In Muscle Hocontrasting

confidence: 80%

Elevated IL-4 and IFN-γ Levels in Muscle Tissue of Patients with Dermatomyositis

Giriş

Durmuş

Yetimler

et al. 2017

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Section: Correlations Between Cytokine Expression Levels In Muscle Hocontrasting

confidence: 80%

Elevated IL-4 and IFN-γ Levels in Muscle Tissue of Patients with Dermatomyositis

Giriş

Durmuş

Yetimler

et al. 2017

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“…These functions are mainly achieved by the binding of mi-RNAs with the 3'-UTR of mRNAs [11]. MiRNAs have recently been implicated in inflammatory responses, sepsis, and, specifically, macrophage activities [9,[12][13][14]. MicroRNA-138 (miR-138) is reported to participate in oncogenesis and axon regeneration, but it is not clear whether miR-138 plays a role in inflammation or sepsis [15,16].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-138 Aggravates Inflammatory Responses of Macrophages by Targeting SIRT1 and Regulating the NF-κB and AKT Pathways

Bai

Zhang

Yang

et al. 2018

Cell Physiol Biochem

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Background/Aims: With increased understanding of sepsis, mortality is decreasing. However, there is still a lack of effective therapeutic strategy. The inflammatory response of macrophages is critical during sepsis. Methods: Macrophages were stimulated with LPS. Western blotting and qRT-PCR were used to detect inflammatory responses. Then, the inhibitor of microRNA-138 was transfected and Western blotting, qRT-PCR, H&E staining and ELISA were used to verify the role of microRNA-138 in inflammation. Then target gene prediction databases were used to predict the potential target of microRNA-138. Both animal and cell models under LPS challenges were established to verify the regulation of SIRT1 and microRNA-138 during inflammation. Results: The present study showed that microRNA-138 was increased in macrophages stimulated with LPS. Additionally, the NF-κB and AKT pathways were both activated. The pre-treatment of microRNA-138 inhibitor decreased inflammatory factors, downregulated the NF-κB pathway, activated the AKT pathway and protected against organ damage in mice challenged with LPS. SIRT1 was demonstrated as a potential target of microRNA-138In macrophages stimulated with LPS, the inhibition effect of microRNA-138 inhibitor on inflammation was lost by SIRT1 siRNA pre-treatment. In the animal model, the protective effect of microRNA-138 antagomir disappeared in SIRT1 knockout mice. Conclusion: We demonstrated that miR-138 participated in the inflammatory process by inhibiting SIRT1 and activating the NF-κB pathway.

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“…Ultimately, this results in impaired inflammation. Along these lines, miR-146a 2/2 mice have enhanced endothelial inflammatory responses (2,7). In addition, thrombin and LPS are inducing the expression of miR-146a that targets caspase recruitment domain-containing protein 10 (Card10), an adaptor protein implicated in the activation of the IKK complex, to reduce inflammation (8,9).…”

Section: Mirnas Target the Receptor Complex Of Nf-kb Pathwaymentioning

confidence: 99%

“…The transcription of all these 3 cell adhesion molecules is driven predominantly by the proinflammatory transcription factor NF-kB (2). The major form of NF-kB is the p65/ p50 heterodimer.…”

mentioning

confidence: 99%

Endothelial microRNAs regulating the NF‐κB pathway and cell adhesion molecules during inflammation

2018

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The surface of endothelial cells is covered with cell adhesion molecules, including E-selectin, intercellular adhesion molecule 1 (ICAM-1), and vascular cell adhesion molecule 1 (VCAM- 1) , that mediate the adhesion and extravasation of leukocytes and play pivotal roles in inflammatory response. microRNAs (miRNAs) regulate the expression of these important cell adhesion molecules through two distinct major mechanisms, namely via modulating the proinflammatory NF-κB pathway, which controls their transcription, and via directly targeting them. The present review highlights the role of various miRNAs in controlling the expression of E-selectin, ICAM-1, and VCAM-1: a type of regulation that can be harnessed for therapeutic prevention of inflammation-associated diseases such as atherosclerosis and sepsis. The roles of secreted miRNAs as paracrine regulators, and cell adhesion molecule-based miRNA delivery are also addressed.-Zhong, L., Simard, M. J., Huot, J. Endothelial microRNAs regulating the NF-κB pathway and cell adhesion molecules during inflammation.

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MiR-146a Regulates Inflammatory Infiltration by Macrophages in Polymyositis/Dermatomyositis by Targeting TRAF6 and Affecting IL-17/ICAM-1 Pathway

Cited by 37 publications

References 40 publications

Elevated IL-4 and IFN-γ Levels in Muscle Tissue of Patients with Dermatomyositis

Elevated IL-4 and IFN-γ Levels in Muscle Tissue of Patients with Dermatomyositis

MicroRNA-138 Aggravates Inflammatory Responses of Macrophages by Targeting SIRT1 and Regulating the NF-κB and AKT Pathways

Endothelial microRNAs regulating the NF‐κB pathway and cell adhesion molecules during inflammation

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