Knocking Down Gm16685 Decreases Liver Granuloma in Murine Schistosomiasis Japonica

Zhao, Ruyu; Tang, Xiaoxue; Lin, Huiyao; Chen, Xing; Xu, Na; Dai, Bingxin; Wang, Pingping; Shao, Wei; Liu, Miao; Shen, Jijia; Deng, Sheng-Qun; Ren, Chao

doi:10.3390/microorganisms11030796

Cited by 3 publications

(1 citation statement)

References 41 publications

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“…On the host side, 759 and 789 differentially expressed lncRNAs are observed in liver and spleen of S. japonicum parasitized mice, respectively [ 182 ]. LncRNA Gm16685 is upregulated during S. japonicum infection, and participates in the pathogenesis throughout schistosomiasis by regulating miR-205-5p [ 183 ]. The involvement of lncRNA H19 in S. japonica has also been corroborated, as it governs the hepatic reaction to Praziquantel therapy against S. japonicum infection through the H19 /miR-130b-3p/ Cyp4a14 axis [ 184 ].…”

Section: Lncrnas In Parasitic Zoonosesmentioning

confidence: 99%

Unveiling the Hidden Regulators: The Impact of lncRNAs on Zoonoses

Xu,

He,

Yang

et al. 2024

IJMS

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Zoonoses are diseases and infections naturally transmitted between humans and vertebrate animals. They form the dominant group of diseases among emerging infectious diseases and represent critical threats to global health security. This dilemma is largely attributed to our insufficient knowledge of the pathogenesis regarding zoonotic spillover. Long non-coding RNAs (lncRNAs) are transcripts with limited coding capacity. Recent technological advancements have enabled the identification of numerous lncRNAs in humans, animals, and even pathogens. An increasing body of literature suggests that lncRNAs function as key regulators in zoonotic infection. They regulate immune-related epigenetic, transcriptional, and post-transcriptional events across a broad range of organisms. In this review, we discuss the recent research progress on the roles of lncRNAs in zoonoses. We address the classification and regulatory mechanisms of lncRNAs in the interaction between host and zoonotic pathogens. Additionally, we explore the surprising function of pathogen-derived lncRNAs in mediating the pathogenicity and life cycle of zoonotic bacteria, viruses, and parasites. Understanding how these lncRNAs influence the zoonotic pathogenesis will provide important therapeutic insights to the prevention and control of zoonoses.

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Section: Lncrnas In Parasitic Zoonosesmentioning

confidence: 99%

Unveiling the Hidden Regulators: The Impact of lncRNAs on Zoonoses

Xu,

He,

Yang

et al. 2024

IJMS

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Chromatin structure around long non-coding RNA (lncRNA) genes inSchistosoma mansonigonads

de Carvalho Augusto,

Quack,

Grevelding

et al. 2024

Preprint

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In this study, we employed a total of eight distinct modifications of histone proteins (H3K23ac, H3K27me3, H3K36me3, H3K4me3, H3K9ac, H3K9me3, H4K12ac, and H4K20me1) to discern the various chromatin colors encompassing lncRNA genes in both mature and immature gonads of the human parasiteSchistosoma mansoni. Our investigation revealed that these chromatin colors exhibit a tendency to aggregate based on the similarities in their metagene shapes, leading to the formation of less than six distinct clusters. Moreover, these clusters can be further grouped according to their resemblances by shape, which are co-linear with specific regions of the genes and potentially associated with transcriptional stages.

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Schistosoma japonicum infection-mediated downregulation of lncRNA Malat1 contributes to schistosomiasis hepatic fibrosis by the Malat1/miR-96/Smad7 pathway

Jiang,

Ye,

Fan

et al. 2024

Parasites Vectors

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Background Schistosoma japonicum infection causes hepatic fibrosis, a primary cause of morbidity and mortality associated with the disease, and effective treatments are still lacking. Long non-coding RNAs (lncRNAs) have been implicated in the pathogenic process of various tissue fibroses. However, the role of lncRNAs in schistosomiasis hepatic fibrosis (HF) is poorly understood. Understanding the role of lncRNAs in schistosomiasis HF will enhance knowledge of disease processes and aid in the discovery of therapeutic targets and diagnostic biomarkers. Methods Differentially expressed lncRNA profiles in primary hepatic stellate cells (HSCs) of mice infected with S. japonicum were identified using high-throughput lncRNA sequencing. Primary HSCs were isolated from infected mice using collagenase digestion and density-gradient centrifugation, cultured in DMEM with 10% fetal bovine serum. Dual-luciferase reporter assays, nuclear cytoplasm fractionation and RIP assays were employed to assess the relationship between Malat1 and miRNA-96. Malat1 lentivirus and ASO-Malat1 were constructed for forced expression and downregulated expression of Malat1. The Malat1-KO mouse was constructed by CRISPR/Cas9 technology. Pathological features of the liver were evaluated by hematoxylin-eosin (HE), Masson’s trichrome staining and immunohistochemistry (IHC). The expression levels of fibrosis-related genes were determined by quantitative real-time PCR (qRT-PCR) and Western blot. Results A total of 1561 differentially expressed lncRNAs were identified between infected and uninfected primary HSCs. Among the top altered lncRNAs, the downregulated Malat1 was observed in infected HSCs and verified by qPCR. Treatment of infected mice with praziquantel (PZQ) significantly increased the Malat1 expression. Elevated Malat1 expression in infected primary HSC reduced the expressions of profibrogenic genes, whereas Malat1 knockdown had the opposite effect. Moreover, Malat1 was found to interact with miR-96, a profibrotic miRNA, by targeting Smad7. Forced Malat1 expression reduced miR-96 levels in infected primary HSCs, attenuating fibrogenesis and showing negative correlation between Malat1 expression and the expression levels of miR-96 and profibrogenic genes α-SMA and Col1α1. Notably, in Malat1-KO mice, knockout of Malat1 aggravates schistosomiasis HF, while restored Malat1 expression in the infected HSCs reduced the expression of profibrogenic genes. Conclusions We demonstrate that lncRNA is involved in regulation of schistosomiasis HF. Elevated lncRNA Malat1 expression in infected HSCs reduces fibrosis via the Malat1/miR-96/Smad7 pathway, thus providing a novel therapeutic target for schistosomiasis HF. Furthermore, Malat1 expression is sensitive to PZQ treatment, thus offering a potential biomarker for assessing the response to chemotherapy. Graphical abstract

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Knocking Down Gm16685 Decreases Liver Granuloma in Murine Schistosomiasis Japonica

Cited by 3 publications

References 41 publications

Unveiling the Hidden Regulators: The Impact of lncRNAs on Zoonoses

Unveiling the Hidden Regulators: The Impact of lncRNAs on Zoonoses

Chromatin structure around long non-coding RNA (lncRNA) genes inSchistosoma mansonigonads

Schistosoma japonicum infection-mediated downregulation of lncRNA Malat1 contributes to schistosomiasis hepatic fibrosis by the Malat1/miR-96/Smad7 pathway

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