Long noncoding RNA SNHG8 accelerates acute gouty arthritis development by upregulating AP3D1 in mice

Gout can affect the quality of life of patients due to monosodium urate monohydrate (MSU) crystals. Numerous studies have proposed that long noncoding RNAs (lncRNAs) regulate gout. We aimed to reveal the function of lncRNA small nucleolar RNA host gene 8 (SNHG8) in acute gouty arthritis (GA). A GA m...

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Veröffentlicht in:Bioengineered 2021-12, Vol.12 (2), p.9803-9815
Hauptverfasser: Fang, Li, Xu, Xiangfeng, Lu, Yao, Wu, Yanying, Li, Jiajia
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Xu, Xiangfeng
Lu, Yao
Wu, Yanying
Li, Jiajia
description Gout can affect the quality of life of patients due to monosodium urate monohydrate (MSU) crystals. Numerous studies have proposed that long noncoding RNAs (lncRNAs) regulate gout. We aimed to reveal the function of lncRNA small nucleolar RNA host gene 8 (SNHG8) in acute gouty arthritis (GA). A GA mouse model was established by injection of MSU into footpads. The levels of SNHG8, miR-542-3p and adaptor-related protein complex 3 subunit delta 1 (AP3D1) in footpads were detected via polymerase chain reaction analysis. Hematoxylin-eosin staining revealed the paw swelling in mice. Enzyme-linked immunosorbent assay and western blot analysis were applied to determine the concentrations of proinflammatory cytokines. SNHG8 expression was identified to be upregulated after MSU treatment. Ablation of SNHG8 decreased the MSU-induced enhancement of paw swelling and foot thickness. In addition, SNHG8 depletion decreased the protein levels of proinflammatory factors in GA mice. Mechanically, SNHG8 was verified to be a sponge of miR-542-3p, and miR-542-3p targeted AP3D1 3ʹ untranslated region. SNHG8 competitively bound with miR-542-3p to upregulate AP3D1 expression. Finally, results of rescue assays illustrated that AP3D1 upregulation offset the SNHG8-mediated inhibition on paw swelling and protein levels of proinflammatory factors in GA mice. In conclusion, SNHG8 accelerates acute GA development by upregulating AP3D1 in an miR-542-3p-dependent way in mice, providing an effective therapeutic approach to treat acute GA.
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Numerous studies have proposed that long noncoding RNAs (lncRNAs) regulate gout. We aimed to reveal the function of lncRNA small nucleolar RNA host gene 8 (SNHG8) in acute gouty arthritis (GA). A GA mouse model was established by injection of MSU into footpads. The levels of SNHG8, miR-542-3p and adaptor-related protein complex 3 subunit delta 1 (AP3D1) in footpads were detected via polymerase chain reaction analysis. Hematoxylin-eosin staining revealed the paw swelling in mice. Enzyme-linked immunosorbent assay and western blot analysis were applied to determine the concentrations of proinflammatory cytokines. SNHG8 expression was identified to be upregulated after MSU treatment. Ablation of SNHG8 decreased the MSU-induced enhancement of paw swelling and foot thickness. In addition, SNHG8 depletion decreased the protein levels of proinflammatory factors in GA mice. Mechanically, SNHG8 was verified to be a sponge of miR-542-3p, and miR-542-3p targeted AP3D1 3ʹ untranslated region. SNHG8 competitively bound with miR-542-3p to upregulate AP3D1 expression. Finally, results of rescue assays illustrated that AP3D1 upregulation offset the SNHG8-mediated inhibition on paw swelling and protein levels of proinflammatory factors in GA mice. In conclusion, SNHG8 accelerates acute GA development by upregulating AP3D1 in an miR-542-3p-dependent way in mice, providing an effective therapeutic approach to treat acute GA.</description><identifier>ISSN: 2165-5979</identifier><identifier>EISSN: 2165-5987</identifier><identifier>DOI: 10.1080/21655979.2021.1995579</identifier><identifier>PMID: 34874227</identifier><language>eng</language><publisher>United States: Taylor &amp; Francis</publisher><subject>Acute Disease ; acute gouty arthritis ; Adaptor Protein Complex 3 - biosynthesis ; Adaptor Protein Complex 3 - genetics ; Adaptor Protein Complex beta Subunits - biosynthesis ; Adaptor Protein Complex beta Subunits - genetics ; Animals ; AP3D1 ; Arthritis, Gouty - genetics ; Arthritis, Gouty - metabolism ; Humans ; Male ; Mice ; miR-542-3p ; Research Paper ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; SNHG8 ; THP-1 Cells ; Up-Regulation</subject><ispartof>Bioengineered, 2021-12, Vol.12 (2), p.9803-9815</ispartof><rights>2021 The Author(s). 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Numerous studies have proposed that long noncoding RNAs (lncRNAs) regulate gout. We aimed to reveal the function of lncRNA small nucleolar RNA host gene 8 (SNHG8) in acute gouty arthritis (GA). A GA mouse model was established by injection of MSU into footpads. The levels of SNHG8, miR-542-3p and adaptor-related protein complex 3 subunit delta 1 (AP3D1) in footpads were detected via polymerase chain reaction analysis. Hematoxylin-eosin staining revealed the paw swelling in mice. Enzyme-linked immunosorbent assay and western blot analysis were applied to determine the concentrations of proinflammatory cytokines. SNHG8 expression was identified to be upregulated after MSU treatment. Ablation of SNHG8 decreased the MSU-induced enhancement of paw swelling and foot thickness. In addition, SNHG8 depletion decreased the protein levels of proinflammatory factors in GA mice. Mechanically, SNHG8 was verified to be a sponge of miR-542-3p, and miR-542-3p targeted AP3D1 3ʹ untranslated region. SNHG8 competitively bound with miR-542-3p to upregulate AP3D1 expression. Finally, results of rescue assays illustrated that AP3D1 upregulation offset the SNHG8-mediated inhibition on paw swelling and protein levels of proinflammatory factors in GA mice. 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SNHG8 competitively bound with miR-542-3p to upregulate AP3D1 expression. Finally, results of rescue assays illustrated that AP3D1 upregulation offset the SNHG8-mediated inhibition on paw swelling and protein levels of proinflammatory factors in GA mice. In conclusion, SNHG8 accelerates acute GA development by upregulating AP3D1 in an miR-542-3p-dependent way in mice, providing an effective therapeutic approach to treat acute GA.</abstract><cop>United States</cop><pub>Taylor &amp; Francis</pub><pmid>34874227</pmid><doi>10.1080/21655979.2021.1995579</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-8850-9519</orcidid><oa>free_for_read</oa></addata></record>
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subjects Acute Disease
acute gouty arthritis
Adaptor Protein Complex 3 - biosynthesis
Adaptor Protein Complex 3 - genetics
Adaptor Protein Complex beta Subunits - biosynthesis
Adaptor Protein Complex beta Subunits - genetics
Animals
AP3D1
Arthritis, Gouty - genetics
Arthritis, Gouty - metabolism
Humans
Male
Mice
miR-542-3p
Research Paper
RNA, Long Noncoding - genetics
RNA, Long Noncoding - metabolism
SNHG8
THP-1 Cells
Up-Regulation
title Long noncoding RNA SNHG8 accelerates acute gouty arthritis development by upregulating AP3D1 in mice
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