Mmu-miR-92a-2-5p targets TLR2 to relieve Schistosoma japonicum-induced liver fibrosis

Zhao, Yumin; Dang, Zhisheng; Chong, Shigui

doi:10.1016/j.intimp.2019.01.007

Cited by 19 publications

(14 citation statements)

References 30 publications

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“…In addition, it was noticed that in ALI rats' lung tissues, TLR2 and AP-1 were suppressed after inhibiting the expression of miR-92a, and the expression of AP-1 was decreased after knocking out the TLR2 gene, suggesting that miR-92a/TLR2/AP-1 might be a signaling axis that exerts marked effects on the occurrence and development of ALI. The regulatory effect of miRNAs on TLR protein has been confirmed in many studies [ 20 ], while only Zhao et al [ 12 ] reported that miR-92a could target the regulation of TLR2 expression. Apart from that, it is well established that AP-1 can be regulated by TLR2.…”

Section: Discussionmentioning

confidence: 99%

“…MiR-92a has also been found to act on development of inflammatory responses in ALI rats, and its inhibition can reduce the secretion of proinflammatory factors and improve inflammatory responses [ 11 ]. MiRNAs are important regulators of Toll-like receptor (TLR) signaling, among which TLR2 has been reported as one of the targets of miR-92a, which can alleviate liver fibrosis caused by Schistosoma japonicum [ 12 ]. In addition, Lai et al [ 13 ] demonstrated that TLR-mediated decrease in miR-92a expression can promote the production of inflammatory cytokines in TLR-induced macrophages.…”

Section: Introductionmentioning

confidence: 99%

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Inhibition Mir-92a Alleviates Oxidative Stress and Apoptosis of Alveolar Epithelial Cells Induced by Lipopolysaccharide Exposure through TLR2/AP-1 Pathway

Cui

Ding

Yao

et al. 2020

BioMed Research International

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Objective. To probe into the role of miR-92a in alleviating oxidative stress and apoptosis of alveolar epithelial cell (AEC) injury induced by lipopolysaccharide (LPS) exposure through the Toll-like receptor (TLR) 2/activator protein-1 (AP-1) pathway. Methods. Acute lung injury (ALI) rat model and ALI alveolar epithelial cell model were constructed to inhibit the expression of miR-92a/TLR2/AP-1 in rat and alveolar epithelial cells (AECs), to detect the changes of oxidative stress, inflammatory response, and cell apoptosis in rat lung tissues and AECs, and to measure the changes of wet-dry weight (W/D) ratio in rat lung tissues. Results. Both inhibition of miR-92a expression and knockout of TLR2 and AP-1 gene could reduce LPS-induced rat ALI, alleviate pulmonary edema, inhibit oxidative stress and inflammatory response, and reduce apoptosis of lung tissue cells. In addition, the TLR2 and AP-1 levels in the lung tissues of ALI rats were noticed to be suppressed when inhibiting the expression of miR-92a, and the AP-1 level was also decreased after the knockout of TLR2 gene. Further, we verified this relationship in AECs and found that inhibition of miR-92a/TLR2/AP-1 also alleviated LPS-induced AEC injury, reduced cell apoptosis, and inhibited oxidative stress and inflammatory response. What is more, like that in rat lung tissue, the phenomenon also existed in AECs, that is, when the expression of miR-92a was inhibited, the expression of TLR2 and AP-1 was inhibited, and silencing TLR2 can reduce the expression level of AP-1. Conclusion. MiR-92a/TLR2/AP-1 is highly expressed in ALI, and its inhibition can improve oxidative stress and inflammatory response and reduce apoptosis of AECs.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Inhibition Mir-92a Alleviates Oxidative Stress and Apoptosis of Alveolar Epithelial Cells Induced by Lipopolysaccharide Exposure through TLR2/AP-1 Pathway

Cui

Ding

Yao

et al. 2020

BioMed Research International

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“…TLR2 may be involved in C. parvum-induced stabilization of iNOS mRNA expression in biliary epithelial cells [13]. Post-transcriptional suppression of TLR4 expression by let-7i has been shown to contribute to immune responses to C. parvum infection in cultured human cholangiocytes, and mu-miR-92a-2-5p, which targets TLR2, relieves Schistosoma japonicum-induced liver fibrosis [6,24].…”

Section: Discussionmentioning

confidence: 99%

Cryptosporidium parvum upregulates miR-942-5p expression in HCT-8 cells via TLR2/TLR4-NF-κB signaling

Zhang

Niu

et al. 2020

Parasites Vectors

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Background: Micro (mi)RNAs are small noncoding RNA molecules that function in RNA silencing and post-transcriptional regulation of gene expression. This study investigated host miRNA activity in the innate immune response to Cryptosporidium parvum infection. Methods: In vitro infection model adopts HCT-8 human ileocecal adenocarcinoma cells infected with C. parvum. The expression of miR-942-5p was estimated using quantitative real-time polymerase chain reaction (qPCR). The TLRs-NF-κB signaling was confirmed by qPCR, western blotting, TLR4-and TLR2-specific short-interfering (si)RNA, and NF-κB inhibition. Results: HCT-8 cells express all known toll-like receptors (TLRs). Cryptosporidium parvum infection of cultured HCT-8 cells upregulated TLR2 and TLR4, and downstream TLR effectors, including NF-κB and suppressed IκBα (nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha). The expression of miR-942-5p was significantly upregulated at 4, 8, 12 and 24 h post-infection, and especially at 8 hpi. The results of TLR4-and TLR2-specific siRNA and NF-κB inhibition showed that upregulation of miR-942-5p was promoted by p65 subunit-dependent TLR2/TLR4-NF-κB pathway signaling. Conclusions: miR-942-5p of HCT-8 cells was significantly upregulated after C. parvum infection, especially at 8 hpi, in response to a p65-dependent TLR2/TLR4-NF-κB signaling. TLR4 appeared to play a dominant role.

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“…During schistosomiasis-associated liver fibrosis, miR-29b-3p is believed to inhibit HSC activation by targeting COL1A1 and COL3A1 in the TGF-β1 signaling pathway [94]. Moreover, another recent study showed that mmu-miR-92a-2-5p inhibits schistosome-induced liver fibrosis in vitro and in vivo by targeting TLR2, but the underlying molecular mechanism remains unclear [95]. TGF-β/SMAD signaling is an important pathway for HSC activation, and the modulatory roles of miRNAs in this signaling pathway further affect schistosomiasis-associated liver fibrosis are summarized in Fig.…”

Section: Anti-fibrogenic Role Of Mirnas In Schistosomiasismentioning

confidence: 99%

The role of microRNAs in the pathogenesis, grading and treatment of hepatic fibrosis in schistosomiasis

et al. 2019

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Schistosomiasis is a prevalent parasitic disease worldwide. The main pathological changes of hepatosplenic schistosomiasis are hepatic granuloma and fibrosis due to worm eggs. Portal hypertension and ascites induced by hepatic fibrosis are usually the main causes of death in patients with chronic hepatosplenic schistosomiasis. Currently, no effective vaccine exists for preventing schistosome infections. For quite a long time, praziquantel (PZQ) was widely used for the treatment of schistosomiasis and has shown benefit in treating liver fibrosis. However, drug resistance and chemical toxicity from PZQ are being increasingly reported in recent years; therefore, new and effective strategies for treating schistosomiasis-induced hepatic fibrosis are urgently needed. MicroRNA (miRNA), a non-coding RNA, has been proved to be associated with the development of many human diseases, including schistosomiasis. In this review, we present a balanced and comprehensive view of the role of miRNAs in the pathogenesis, grading, and treatment of schistosomiasis-associated hepatic fibrosis. The multiple regulatory roles of miRNAs, such as promoting or inhibiting the development of liver pathology in murine schistosomiasis are also discussed in depth. Additionally, miRNAs may serve as candidate biomarkers for diagnosing liver pathology of schistosomiasis and as novel therapeutic targets for treating schistosomiasis-associated hepatic fibrosis.

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Mmu-miR-92a-2-5p targets TLR2 to relieve Schistosoma japonicum-induced liver fibrosis

Cited by 19 publications

References 30 publications

Inhibition Mir-92a Alleviates Oxidative Stress and Apoptosis of Alveolar Epithelial Cells Induced by Lipopolysaccharide Exposure through TLR2/AP-1 Pathway

Inhibition Mir-92a Alleviates Oxidative Stress and Apoptosis of Alveolar Epithelial Cells Induced by Lipopolysaccharide Exposure through TLR2/AP-1 Pathway

Cryptosporidium parvum upregulates miR-942-5p expression in HCT-8 cells via TLR2/TLR4-NF-κB signaling

The role of microRNAs in the pathogenesis, grading and treatment of hepatic fibrosis in schistosomiasis

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