SHIP‐1, a target of miR‐155, regulates endothelial cell responses in lung fibrosis

Tang, Haiying; Mao, Jingsong; Ye, Xujun; Zhang, Fengrui; Kerr, William G.; Zheng, Tao; Zhu, Zhou

doi:10.1096/fj.201902063r

Cited by 28 publications

(18 citation statements)

References 48 publications

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“…Similar observations were obtained in monocytes from patients with rheumatoid arthritis (19), whereby overexpression of miR-155 reverses the inhibitory effect of triptolide on LPS-induced interleukin (IL)-6 and tumor necrosis factor-α production, and antagonizes the effect of triptolide on Src homology 2-containing inositol phosphatase-1 (SHIP-1), which is a target of miR-155 and functions as a potent inhibitor of several inflammatory pathways (71). Thus, it has been proposed that triptolide inhibits miR-155 expression, which negatively affects its downstream target, SHIP-1, and suppresses the inflammatory response stimulated by LPS.…”

Section: Triptolide Modulates the Expression Of Mirnassupporting

confidence: 66%

MicroRNAs as crucial mediators in the pharmacological activities of triptolide (Review)

Zhou¹,

Chang

Han

et al. 2021

Exp Ther Med

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Triptolide is the main bioactive constituent isolated from the Chinese herb Tripterygium wilfordii Hook F., which possesses a variety of pharmacological properties. MicroRNAs (miRNAs/miRs) are short non-coding RNAs that regulate gene expression post-transcriptionally. miRNAs are implicated in several intracellular processes, whereby their dysregulation contributes to pathogenesis of various diseases. Thus, miRNAs have great potential as biomarkers and therapeutic targets for diseases, and are implicated in drug treatment. Previous studies have reported that specific miRNAs are targeted, and their expression levels can be altered following exposure to triptolide. Thus, miRNAs are emerging as crucial mediators in the pharmacological activities of triptolide. The present review summarizes current literature on miRNAs as target molecules in the pharmacological activities of triptolide, including antitumor, anti-inflammatory, immunosuppressive, renal protective, cardioprotective, antiangiogenesis activities and multiorgan toxicity effects. In addition, the diverse signaling pathways involved are discussed to provide a comprehensive understanding of the underlying molecular mechanisms of triptolide in the regulation of target miRNAs.

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Section: Triptolide Modulates the Expression Of Mirnassupporting

confidence: 66%

MicroRNAs as crucial mediators in the pharmacological activities of triptolide (Review)

Zhou¹,

Chang

Han

et al. 2021

Exp Ther Med

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“…In the searching for the most prominent targets of miR-155 in odontoblast, our bioinformatics results con rmed that SHIP1 was one of the most important factors in dental in ammation. Many reports have stated that SHIP1 is a key factor for miR-155 regulation in in ammation, brosis, and other immune processes [14,21,35]. We veri ed that miR-155 directly interacted and regulated the expression of SHIP1 in pulpal in ammation.…”

Section: Discussionmentioning

confidence: 65%

MicroRNA-155 Expression Is Associated With Pulpitis Progression By Targeting SHIP1

Guo

et al. 2021

Preprint

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Pulpitis is a commonly seen oral inflammation condition in clinical practice, it can cause much pain for the patient and may induce infections in other systems. Much is still unknown for the pathogenic mechanism of pulpitis. In this work, we discovered that the expression of miR-155 was associated with dental pulpal inflammation both in vivo and in vitro. Experiments on odontoblast cell line MDPC-23 showed miR-155 could act as a positive regulator by increasing the production of pro-inflammatory cytokines IL-1β and IL-6 during inflammatory responses, whereas knockdown of miR-155 can reverse the effects. Bioinformatics analysis demonstrated that SHIP1 is a direct target of miR-155 in odontoblasts, this result was further verified at both mRNA and protein level. Inhibition of miR-155 resulted in the downregulation of inflammation factors, while co-transfection of si-SHIP1 and miR-155 inhibitor promoted the inflammatory responses. Treatment with miR-155 mimic or si-SHIP1 up-regulated the protein level of p-PI3K and p-AKT. By contrast, miR-155 inhibitor exerted the opposite effects. miR-155 mimics could upregulated the gene expression of IL-1β and IL-6. Co-transfection of LY294002 and miR-155 mimic attenuated the inflammatory responses. Consistent with in vitro results, miR-155-/- mice could alleviate inflammatory response, as well as decrease the activation of p-PI3K and p-AKT, whereas increase the activation of SHIP1. In conclusion, these data revealed a novel role for miR-155 in regulation of dental pulpal inflammatory response by targeting SHIP1 through PI3K/AKT signaling pathway.

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“…[ 47 ] Furthermore, phosphoinositide 3 kinase, which participates in anti-apoptotic pathway in neutrophils, [ 54 ] would be dephosphorylated by SHP-1 via its association with the regulatory p85 subunit. [ 55 , 56 ] Neutrophil survival is regulated by finely-balanced interactions between pro-apoptotic and survival signals, and SHP-1 could be an important regulator in these processes. [ 57 ] Further studies will be awaited to intensively dissect these possible mechanisms.…”

Section: Siglec-9 As a Regulator Of Neutrophil Apoptosis And Autophagymentioning

confidence: 99%

Sialic acid-binding immunoglobulin-like lectin 9 as a potential therapeutic target for chronic obstructive pulmonary disease

Chen

et al. 2021

Chinese Medical Journal

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Chronic obstructive pulmonary disease (COPD) has become the third-leading cause of death worldwide, which is a severe economic burden to the healthcare system. Chronic bronchitis is the most common condition that contributes to COPD, both locally and systemically. Neutrophilic inflammation predominates in the COPD airway wall and lumen. Logically, repression of neutrophilia is an essential fashion to COPD treatment. However, currently available anti-neutrophilic therapies provide little benefit in COPD patients and may have serious side effects. Thus, there is an urgent need to explore an effective and safe anti-neutrophilic approach that might delay progression of the disease. Sialic acid-binding immunoglobulin-like lectin (Siglec)-9 is a member of the Siglec cell surface immunoglobulin family. It is noteworthy that Siglec-9 is highly expressed on human neutrophils and monocytes. Ligation of Siglec-9 by chemical compounds or synthetic ligands induced apoptosis and autophagic-like cell death in human neutrophils. Furthermore, administration of antibody to Siglec-E, mouse functional ortholog of Siglec-9, restrained recruitment and activation of neutrophils in mouse models of airway inflammation in vivo . Given the critical role that neutrophils play in chronic bronchitis and emphysema, targeting Siglec-9 could be beneficial for the treatment of COPD, asthma, fibrosis, and related chronic inflammatory lung diseases.

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SHIP‐1, a target of miR‐155, regulates endothelial cell responses in lung fibrosis

Cited by 28 publications

References 48 publications

MicroRNAs as crucial mediators in the pharmacological activities of triptolide (Review)

MicroRNAs as crucial mediators in the pharmacological activities of triptolide (Review)

MicroRNA-155 Expression Is Associated With Pulpitis Progression By Targeting SHIP1

Sialic acid-binding immunoglobulin-like lectin 9 as a potential therapeutic target for chronic obstructive pulmonary disease

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