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- Publisher Website: 10.1042/CS20220537
- Scopus: eid_2-s2.0-85149154238
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Article: The long noncoding RNA Meg3 mediates TLR4-induced inflammation in experimental obstructive nephropathy
Title | The long noncoding RNA Meg3 mediates TLR4-induced inflammation in experimental obstructive nephropathy |
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Authors | |
Issue Date | 1-Mar-2023 |
Publisher | Portland Press |
Citation | Clinical Science, 2023, v. 137, n. 5, p. 317-331 How to Cite? |
Abstract | Kidney inflammation contributes to the progression of chronic kidney disease (CKD). Modulation of Toll-like receptor 4 (TLR4) signaling is a potential therapeutic strategy for this pathology, but the regulatory mechanisms of TLR4 signaling in kidney tubular inflammation remains unclear. Here, we demonstrated that tubule-specific deletion of TLR4 in mice conferred protection against obstruction-induced kidney injury, with reduction in inflammatory cytokine production, macrophage infiltration and kidney fibrosis. Transcriptome analysis revealed a marked down-regulation of long noncoding RNA (lncRNA) Meg3 in the obstructed kidney from tubule-specific TLR4 knockout mice compared with wild-type control. Meg3 was also induced by lipopolysaccharide in tubular epithelial cells via a p53-dependent signaling pathway. Silencing of Meg3 suppressed LPS-induced cytokine production of CCL-2 and CXCL-2 and the activation of p38 MAPK pathway in vitro and ameliorated kidney fibrosis in mice with obstructive nephropathy. Together, these findings identify a proinflammatory role of lncRNA Meg3 in CKD and suggest a novel regulatory pathway in TLR4-driven inflammatory responses in tubular epithelial cells. |
Persistent Identifier | http://hdl.handle.net/10722/338821 |
ISSN | 2021 Impact Factor: 6.876 2020 SCImago Journal Rankings: 1.910 |
DC Field | Value | Language |
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dc.contributor.author | Yiu, Wai Han | - |
dc.contributor.author | Lok, Sarah WY | - |
dc.contributor.author | Xue, Rui | - |
dc.contributor.author | Chen, Jiaoyi | - |
dc.contributor.author | Lai, Kar Neng | - |
dc.contributor.author | Lan, Hui Yao | - |
dc.contributor.author | Tang, Sydney CW | - |
dc.date.accessioned | 2024-03-11T10:31:48Z | - |
dc.date.available | 2024-03-11T10:31:48Z | - |
dc.date.issued | 2023-03-01 | - |
dc.identifier.citation | Clinical Science, 2023, v. 137, n. 5, p. 317-331 | - |
dc.identifier.issn | 0143-5221 | - |
dc.identifier.uri | http://hdl.handle.net/10722/338821 | - |
dc.description.abstract | <p>Kidney inflammation contributes to the progression of chronic kidney disease (CKD). Modulation of Toll-like receptor 4 (TLR4) signaling is a potential therapeutic strategy for this pathology, but the regulatory mechanisms of TLR4 signaling in kidney tubular inflammation remains unclear. Here, we demonstrated that tubule-specific deletion of TLR4 in mice conferred protection against obstruction-induced kidney injury, with reduction in inflammatory cytokine production, macrophage infiltration and kidney fibrosis. Transcriptome analysis revealed a marked down-regulation of long noncoding RNA (lncRNA) Meg3 in the obstructed kidney from tubule-specific TLR4 knockout mice compared with wild-type control. Meg3 was also induced by lipopolysaccharide in tubular epithelial cells via a p53-dependent signaling pathway. Silencing of Meg3 suppressed LPS-induced cytokine production of CCL-2 and CXCL-2 and the activation of p38 MAPK pathway in vitro and ameliorated kidney fibrosis in mice with obstructive nephropathy. Together, these findings identify a proinflammatory role of lncRNA Meg3 in CKD and suggest a novel regulatory pathway in TLR4-driven inflammatory responses in tubular epithelial cells.</p> | - |
dc.language | eng | - |
dc.publisher | Portland Press | - |
dc.relation.ispartof | Clinical Science | - |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
dc.title | The long noncoding RNA Meg3 mediates TLR4-induced inflammation in experimental obstructive nephropathy | - |
dc.type | Article | - |
dc.identifier.doi | 10.1042/CS20220537 | - |
dc.identifier.scopus | eid_2-s2.0-85149154238 | - |
dc.identifier.volume | 137 | - |
dc.identifier.issue | 5 | - |
dc.identifier.spage | 317 | - |
dc.identifier.epage | 331 | - |
dc.identifier.eissn | 1470-8736 | - |
dc.identifier.issnl | 0143-5221 | - |