Glucocorticoid treatment inhibits intracerebral hemorrhage-induced inflammation by targeting the microRNA-155/SOCS-1 signaling pathway

Xu, Hongfei; Fang, Xiaoyun; Zhu, Shuguang; Xu, Xue‐Hua; Zhang, Zhixiang; Wang, Zufeng; Zhao, Ziqin; Ding, Yujie J.; Tao, Luyang

doi:10.3892/mmr.2016.5716

Cited by 18 publications

(5 citation statements)

References 42 publications

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“…Previous studies have reported that SOCS1 activates associated inflammatory molecules as a potent inhibitor of the production and release of cytokines ( 34 – 36 ). It is well established that miR-155 confers competitive fitness to regulatory T cells by targeting SOCS1 ( 37 ). In addition, it was previously confirmed that miR-155 targets SOCS1 to activate the interleukin-6/Janus kinase/signal transducer and activator of transcription 3 signaling pathway for T helper 17 cell differentiation ( 38 ).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of microRNA-155 ameliorates cardiac fibrosis in the process of angiotensin II-induced cardiac remodeling

Wei

Yan

et al. 2017

Molecular Medicine Reports

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Cardiac fibrosis triggered by pressure overload represents one of the major challenges in the treatment of cardiovascular diseases. MicroRNA (miRNA/miR)-155, a member of the small RNA family, has previously been demonstrated to be associated with cardiac inflammation. However, the effect of miR-155 on cardiac fibrosis induced by angiotensin II (Ang II), particularly in cardiac fibroblasts, requires further investigation. The present study aimed to investigate the effect of miR-155 in Ang II-induced cardiac fibrosis using animal models and cardiac fibroblasts. Animal models were established in male miR-155−/− and wild-type (WT) C57Bl/6J mice (10–12 weeks old) by Ang II infusion using subcutaneously implanted minipumps. After 8 weeks of Ang II infusion, the results demonstrated that the deletion of miR-155 in mice markedly ameliorated ventricular remodeling compared with WT mice, as demonstrated by restricted inflammatory responses, decreased heart size, improved cardiac function and reduced myocardial fibrosis. In vitro, overexpression of miR-155 in cardiac fibroblasts led to significantly increased fibroblast to myofibroblast transformation. However, this effect was abrogated by miR-155 silencing. In conclusion, the results of the present study indicate that genetic loss of miR-155 in mice ameliorates cardiac fibrotic remodeling following pressure overload. Therefore, inhibiting miR-155 may have potential as an adjunct to reduce cardiac inflammation in the treatment of cardiac fibrosis.

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Section: Discussionmentioning

confidence: 99%

Inhibition of microRNA-155 ameliorates cardiac fibrosis in the process of angiotensin II-induced cardiac remodeling

Wei

Yan

et al. 2017

Molecular Medicine Reports

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“…The regulatory relationship between miR-155 and SOCS1 has been proved in several types of diseases. miR-155/SOCS-1 signaling pathway is closely involved in the suppression of intracerebral hemorrhage-induced inflammation by glucocorticoid (Xu et al, 2016). miR-155 influenced the inflammation response via SOCS1 in atherogenesis (Yang et al, 2015;Ye et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

Down-regulation of microRNA-155 suppressed Candida albicans induced acute lung injury by activating SOCS1 and inhibiting inflammation response

Gong

Lin

et al. 2022

J Microbiol.

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Acute lung injury caused byCandida albicans could result in high mortality and morbidity. MicroRNA-155 (miR-155) and suppressor of cytokine signaling 1 (SOCS1) have been believed to play a key in the regulation of inflammatory response. Whether miR-155/SOCS1 axis could regulate the acute lung injury caused by C. albicans has not been reported. The acute lung injury animal model was established with acute infection of C. albicans. miR-155 inhibitor, miR-155 mimic, and sh-SOCS1 were constructed. The binding site between miR-155 and SOCS1 was identified with dual luciferase reporter assay. Knockdown of miR-155 markedly inhibited the germ tube formation of C. albicans. Knockdown of miR-155 significantly up-regulated the expression of SOCS1, and the binding site between miR-155 and SOCS1 was identified. Knockdown of miR-155 improved the acute lung injury, suppressed inflammatory factors and fungus loading through SOCS1. Knockdown of SOCS1 greatly reversed the influence of miR-155 inhibitor on the cell apoptosis in vitro. The improvement of acute lung injury caused by C. albicans, suppression of inflammatory response and C. albicans infection, and inhibitor of cell apoptosis were achieved by knocking down miR-155 through SOCS1. This research might provide a new thought for the prevention and treatment of acute lung injury caused by C. albicans through targeting miR-155/SOCS1 axis.

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“…Dexamethasone-mediated alleviation of neuroinflammation in post-ICH mice is associated with a reduction in miR-155 and an increase in suppressor of cytokine signaling (SOCS-1) expression. Additional experiments have demonstrated that miR−155 inhibits SOCS−1 expression in astrocytes, suggesting that miR-155 might regulate astrocyte inflammatory functions by targeting astrocytic SOCS-1 ( 104 ). However, studies on miRNAs and astrocytes after ICH are scarce, and further exploration is required in this field.…”

Section: Mechanism Of Microrna In Modulating Neuroinflammation After Ichmentioning

confidence: 99%

MicroRNAs modulate neuroinflammation after intracerebral hemorrhage: Prospects for new therapy

Xia

Zheng²,

Feng³

et al. 2022

Front. Immunol.

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Intracerebral hemorrhage (ICH) is the most common subtype of hemorrhagic stroke. After ICH, blood components extravasate from vessels into the brain, activating immune cells and causing them to release a series of inflammatory mediators. Immune cells, together with inflammatory mediators, lead to neuroinflammation in the perihematomal region and the whole brain, and neuroinflammation is closely related to secondary brain injury as well as functional recovery of the brain. Despite recent progress in understanding the pathophysiology of ICH, there is still no effective treatment for this disease. MicroRNAs (miRNAs) are non-coding RNAs 17–25 nucleotides in length that are generated naturally in the human body. They bind complementarily to messenger RNAs and suppress translation, thus regulating gene expression at the post-transcriptional level. They have been found to regulate the pathophysiological process of ICH, particularly the neuroinflammatory cascade. Multiple preclinical studies have shown that manipulating the expression and activity of miRNAs can modulate immune cell activities, influence neuroinflammatory responses, and ultimately affect neurological functions after ICH. This implicates the potentially crucial roles of miRNAs in post-ICH neuroinflammation and indicates the possibility of applying miRNA-based therapeutics for this disease. Thus, this review aims to address the pathophysiological roles and molecular underpinnings of miRNAs in the regulation of neuroinflammation after ICH. With a more sophisticated understanding of ICH and miRNAs, it is possible to translate these findings into new pharmacological therapies for ICH.

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Glucocorticoid treatment inhibits intracerebral hemorrhage-induced inflammation by targeting the microRNA-155/SOCS-1 signaling pathway

Cited by 18 publications

References 42 publications

Inhibition of microRNA-155 ameliorates cardiac fibrosis in the process of angiotensin II-induced cardiac remodeling

Inhibition of microRNA-155 ameliorates cardiac fibrosis in the process of angiotensin II-induced cardiac remodeling

Down-regulation of microRNA-155 suppressed Candida albicans induced acute lung injury by activating SOCS1 and inhibiting inflammation response

MicroRNAs modulate neuroinflammation after intracerebral hemorrhage: Prospects for new therapy

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