Injured liver-released miRNA-122 elicits acute pulmonary inflammation via activating alveolar macrophage TLR7 signaling pathway

Li, Han; Liang, Hongwei; Jin, Fangfang; Yan, Xin; Xu, Guifang; Hu, Huanhuan; Liang, Gaoli; Zhan, Shoubin; Hu, Xiuting; Zhao, Quan; Liu, Yuan; Jiang, Zhuhua; Zhang, Chenyu; Chen, Xi; Zen, Ke

doi:10.1073/pnas.1814139116

Cited by 68 publications

(66 citation statements)

References 45 publications

(56 reference statements)

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“…Recent in vivo data demonstrate that miR--122 released from the injured liver can induce acute lung inflammation by activating alveolar macrophages. 20 In our studies there was not a significant decrease in lung miR--122 following liver microRNA depletion. In contrast to the kidney, this suggests that microRNA transfer from the liver to the lung is not significant in the healthy uninjured state.…”

Section: Discussioncontrasting

confidence: 57%

Transfer of hepatocellular microRNA regulates cytochrome P450 2E1 in renal tubular cells

Matthews

Morrison

Tranter

et al. 2020

Preprint

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Extracellular microRNAs have been demonstrated to have the ability to enter kidney tubular cells and modify gene expression. We have used a Dicer--hepatocyte--specific microRNA conditional knock--out (Dicer--CKO) mouse to investigate functional microRNA transfer from liver to kidney under physiological conditions and in the context of drug toxicity. Dicer--CKO mice demonstrated a time-dependent decrease in the hepatocyte--derived microRNA, miR--122, in the kidney in the absence of other microRNA changes. During hepatotoxicity, miR--122 increased in kidney tubular cells; this was abolished in Dicer--CKO mice. Depletion of hepatocyte microRNAs increased expression and activity of the miR--122 target --cytochrome (CYP) P450 2E1 --in the kidney. Serum extracellular vesicles (ECVs) from mice with hepatotoxicity increased proximal tubular cell miR--122 and prevented cisplatin proximal tubular cell toxicity. miR--122 also increased in urinary ECVs during hepatotoxicity in humans.Transfer of microRNA was not restricted to liver injury -we detected miR--499 release with murine cardiac injury, and this correlated with an increase in the kidney. In summary, a physiological transfer of microRNA to the kidney exists, which is increased by liver injury. Regulation of renal drug response due to signalling by microRNA of hepatic origin represents a new paradigm for understanding and preventing nephrotoxicity.

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Section: Discussioncontrasting

confidence: 57%

Transfer of hepatocellular microRNA regulates cytochrome P450 2E1 in renal tubular cells

Matthews

Morrison

Tranter

et al. 2020

Preprint

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“…At the same time, Herschman and his colleagues revealed a specific cDNA which encoded a protein with a foretold structure similar to COX-1during the analysis of phorbol-ester-induced genes in Swiss 3T3 cells 58 and also explained that the product of this gene is a cyclooxygenase enzyme 59 which initiation was inhibited by dexamethasone 60 . Correspondingly, revealing results are also showed in cultured rat mesangial cells 61 , mouse fibroblasts 62 , RAW 264.7 cells 63 , the ovary 64,65 , rat alveolar macrophages 66,67 and other cell types 68 .…”

Section: The Development Of Field and Discovery Of Cox-2mentioning

confidence: 60%

Untitled

2020

IJPSR

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NSAIDs (Non-steroidal anti-inflammatory drugs) show its effect by preventing prostaglandin synthesis, which reasons ulcer complications and mucosal damage all over the gastrointestinal tract. The world"s most accepted drug was aspirin for treatment of pain and inflammation without knowing that it has the ability to inhibit prostaglandin production by inhibiting the cyclooxygenase enzyme for the treatment of pain and inflammation, until the late 1970s. The discovery of cyclo-oxygenase isoenzyme (COX-1 and COX-2), and their distinct function leads to the development of COX-1 and COX-2 selective inhibitors without any gastrointestinal toxicity. Initial intimations of the second form of cyclooxygenase (COX-2), which has different sensitivity for other drugs like aspirin, finally accompanied in a stimulating period of cyclooxygenase inhibitor discovery, concluding in the overview of an absolutely new generation of antiinflammatory drugs. The aim of this paper is to review the development of COX-1 and COX-2 inhibitors. This paper also reviews that, what are the importance and history of natural products in the treatment of inflammation as COX-1 and COX-2 inhibitor. INTRODUCTION: Responsive phase of hyperemia and exudation of blood vessels consequences into inflammation, which leads swelling, consequent redness, heat, and pain in the tissue due to bacterial attack and many more causes like chemical hazards or physical injury 1. Inflammation is a tissue reaction by the body against damage, which comprises a multifaceted display of enzyme initiation, arbitrator issue, cell immigration, extravasations of fluid, repair, and breakdown of tissue 2 .

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“…MicroRNAs (miRNAs) are short, conserved, non-coding RNA molecules with the potential to regulate mRNA stability and/or translation (Seeley et al, 2018). A number of miRNAs such as miR-302, miR-155, miR-223, miR-146, and miR-122 have demonstrated to be essential in the regulation of macrophage activity and innate immune responses (Rothchild et al, 2016;Liu et al, 2012;Wang et al, 2019aWang et al, , 2019b. Nevertheless, previous studies mainly center on the effect of miRNA on inflammatory signaling.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-127 Promotes Anti-microbial Host Defense through Restricting A20-Mediated De-ubiquitination of STAT3

Liu¹,

Mao²,

Kang³

et al. 2020

iScience

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The increasing rising of multiple drug-resistant Staphylococcus aureus has become a major public health concern, underscoring a pressing need for developing therapies essentially based on the understanding of host defensive mechanism. In the present study, we showed that microRNA (miR)-127 played a key role in controlling bacterial infection and conferred a profound protection against staphylococcal pneumonia. The protective effect of miR-127 was largely dependent on its regulation of macrophage bactericidal activity and the generation of IL-22, IL-17, and anti-microbial peptides (AMPs), the pathway primarily driven by STAT3. Importantly, we revealed that the ubiquitin-editing enzyme A20, a genuine target of miR-127, specifically interacted with and repressed K63-ubiquitination of STAT3, thereby compromising its phosphorylation upon bacterial infection. Thus, our data not only identify miR-127 as a non-coding molecule with anti-bacterial activity but also delineate an unappreciated mechanism whereby A20 regulates STAT3-driven anti-microbial signaling via modulating its ubiquitination.

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Injured liver-released miRNA-122 elicits acute pulmonary inflammation via activating alveolar macrophage TLR7 signaling pathway

Cited by 68 publications

References 45 publications

Transfer of hepatocellular microRNA regulates cytochrome P450 2E1 in renal tubular cells

Transfer of hepatocellular microRNA regulates cytochrome P450 2E1 in renal tubular cells

Untitled

MicroRNA-127 Promotes Anti-microbial Host Defense through Restricting A20-Mediated De-ubiquitination of STAT3

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