MicroRNA-24-3p alleviates hepatic ischemia and reperfusion injury in mice through the repression of STING signaling

Shen, Ai; Zheng, Daofeng; Luo, Yunhai; Mou, Tong; Chen, Qingsong; Huang, Zuotian; Wu, Zhongjun

doi:10.1016/j.bbrc.2019.10.182

Cited by 44 publications

(31 citation statements)

References 32 publications

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“…Functionally, we further demonstrated that overexpression of miR-24-3p remarkedly IL-1β-induced in ammation, caspase-3 activity and cartilage ECM degradation in chondrocytes. Consistent with our data, miR-24-3p has been reported to exert protective effects against ischemia/reperfusion (I/R) injury [14,15] and hepatic I/R process [16]. On the contrary, miR-24-3p upregulation could promote intervertebral disc degeneration through IGFBP5 and the ERK signaling pathway [25].…”

Section: Discussionsupporting

confidence: 89%

“…Similarly, Shen et al [16] demonstrated that miR-24-3p may ameliorate in ammatory response and cellular apoptosis in hepatic I/R process, which might be a potential therapeutic target for preventing liver I/R development and progression. Interestingly, a recent study by Ragni et al [17] who pointed that miR-24-3p was involved in adipose-derived mesenchymal stem cells (ASCs) regulating cell homeostasis and regenerative pathways in an OA-resembling environment.…”

Section: Introductionmentioning

confidence: 93%

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MiR-24-3p Attenuates IL-1β-Induced Chondrocyte Injury Associated With Osteoarthritis by Targeting BCL2L12

Xu¹,

Qian

Ren

2020

Preprint

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Background: Osteoarthritis (OA) is a chronic and degenerative joint disease prevalent in the elderly. MiR-24-3p has been reported to be involved in an OA-resembling environment. However, the functional role and underlying mechanism of miR-24-3p in chondrocyte injury associated with OA remains unknown. Methods: The expression of miR-24-3p was determined in OA cases and control patients, as well as IL-1β-stimulated chondrocyte cell line CHON-001 using reverse transcription quantitative PCR analysis. Cell viability was analyzed by CCK-8 assay. Apoptosis status was assessed by caspase-3 activity detection. The pro-inflammatory cytokines (TNF-α and IL-18) were determined using ELISA assay. The association between miR-24-3p and BCL2L12 was confirmed by luciferase reporter assay.Results: We first observed that miR-24-3p expression level was lower in the OA cases than in the control patients and IL-1β decreased the expression of miR-24-3p in the chondrocyte CHON-001. Functionally, overexpression of miR-24-3p significantly attenuated IL-1β-induced chondrocyte injury, as reflected by increased cell viability, decreased caspase-3 activity, pro-inflammatory cytokines (TNF-α and IL-18). Western blot analysis showed that overexpression of miR-24-3p weakened IL-1β-induced cartilage degradation, as reflected by reduction of MMP13 (Matrix Metalloproteinase-13) and ADAMTS5 (A Disintegrin And Metalloproteinase with Thrombospondin Motifs-5) protein expression, as well as markedly elevation of COL2A1 (collagen type II). Importantly, BCL2L12 was demonstrated to be a target of miR-24-3p. BCL2L12 knockdown imitated, while overexpression significantly abrogated the protective effects of miR-24-3p against IL-1β-induced chondrocyte injury.Conclusions: In conclusion, our work provides important insight into targeting miR-24-3p/BCL2L12 axis in OA therapy.

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 93%

MiR-24-3p Attenuates IL-1β-Induced Chondrocyte Injury Associated With Osteoarthritis by Targeting BCL2L12

Xu¹,

Qian

Ren

2020

Preprint

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“…A top hit was a conserved micro-RNA miR-24, which has been shown to post-transcriptionally regulate endogenous STING in Rattus norvegicus epithelium cells [30]. More recently, a study of liver ischemia reperfusion injury reported critical downregulation of STING via miR-24-3p [31]. MiR-24-2 (encoded by the Mirn23a locus) was also increased in our RNAseq data set from Brucella-infected macrophages [17].…”

Section: Plos Pathogensmentioning

confidence: 70%

Brucella suppress STING expression via miR-24 to enhance infection

et al. 2020

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Brucellosis, caused by a number of Brucella species, remains the most prevalent zoonotic disease worldwide. Brucella establish chronic infections within host macrophages despite triggering cytosolic innate immune sensors, including Stimulator of Interferon Genes (STING), which potentially limit infection. In this study, STING was required for control of chronic Brucella infection in vivo. However, early during infection, Brucella down-regulated STING mRNA and protein. Down-regulation occurred post-transcriptionally, required live bacteria, the Brucella type IV secretion system, and was independent of host IRE1-RNase activity. STING suppression occurred in MyD88-/- macrophages and was not induced by Toll-like receptor agonists or purified Brucella lipopolysaccharide (LPS). Rather, Brucella induced a STING-targeting microRNA, miR-24-2, in a type IV secretion system-dependent manner. Furthermore, STING downregulation was inhibited by miR-24 anti-miRs and in Mirn23a locus-deficient macrophages. Failure to suppress STING expression in Mirn23a-/- macrophages correlated with diminished Brucella replication, and was rescued by exogenous miR-24. Mirn23a-/- mice were also more resistant to splenic colonization one week post infection. Anti-miR-24 potently suppressed replication in wild type, but much less in STING-/- macrophages, suggesting most of the impact of miR-24 induction on replication occurred via STING suppression. In summary, Brucella sabotages cytosolic surveillance by miR-24-dependent suppression of STING expression; post-STING activation “damage control” via targeted STING destruction may enable establishment of chronic infection.

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“…CDNs, cyclic dinucleotides; cGAS, cyclic GMP-AMP synthase; ER, endoplasmic reticulum; TBK1, TANK-binding kinase 1; IRF3, interferon regulatory factor 3; NF-κB, nuclear factor-κB recently found to regulate STING expression. miR-210 [19], miR24-3p [20] and MiR-576-3p [21] could inhibit STING expression at both translational and protein levels. In contrast, miR29a and miR378b could activate STING signaling [22].…”

Section: Regulation and Modification Of Sting Signalingmentioning

confidence: 96%

Cytosolic sensor STING in mucosal immunity: a master regulator of gut inflammation and carcinogenesis

Zhou

Xia

et al. 2021

J Exp Clin Cancer Res

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The stimulator of interferon genes (STING) connects microbial cytosolic sensing with host cell effector functions. STING signaling plays a central role in cyclic dinucleotides (CDNs) and DNA sensing to induce secretion of interferons and pro-inflammatory mediators. Although activated STING signaling favors antimicrobial progress and facilitates mucosal would healing, its role in mucosal immunity and gut homeostasis is paradoxical, ranging from positive and negative effects within the gut. In our review, we summarize recent advance of STING signaling in gut homeostasis and inflammation, especially focusing on its molecular basis in mucosal immune response. Deep understanding of the regulatory mechanisms of intestinal STING pathway could promote clinical manipulation of this fundamental signaling as a promising immunomodulatory therapy.

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MicroRNA-24-3p alleviates hepatic ischemia and reperfusion injury in mice through the repression of STING signaling

Cited by 44 publications

References 32 publications

MiR-24-3p Attenuates IL-1β-Induced Chondrocyte Injury Associated With Osteoarthritis by Targeting BCL2L12

MiR-24-3p Attenuates IL-1β-Induced Chondrocyte Injury Associated With Osteoarthritis by Targeting BCL2L12

Brucella suppress STING expression via miR-24 to enhance infection

Cytosolic sensor STING in mucosal immunity: a master regulator of gut inflammation and carcinogenesis

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