Ablation of Gadd45β ameliorates the inflammation and renal fibrosis caused by unilateral ureteral obstruction
The growth arrest and DNA damage‐inducible beta (Gadd45β) protein have been associated with various cellular functions, but its role in progressive renal disease is currently unknown. Here, we examined the effect of Gadd45β deletion on cell proliferation and apoptosis, inflammation, and renal fibros...
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| description | The growth arrest and DNA damage‐inducible beta (Gadd45β) protein have been associated with various cellular functions, but its role in progressive renal disease is currently unknown. Here, we examined the effect of Gadd45β deletion on cell proliferation and apoptosis, inflammation, and renal fibrosis in an early chronic kidney disease (CKD) mouse model following unilateral ureteral obstruction (UUO). Wild‐type (WT) and Gadd45β‐knockout (KO) mice underwent either a sham operation or UUO and the kidneys were sampled eight days later. A histological assay revealed that ablation of Gadd45β ameliorated UUO‐induced renal injury. Cell proliferation was higher in Gadd45β KO mouse kidneys, but apoptosis was similar in both genotypes after UUO. Expression of pro‐inflammatory cytokines after UUO was down‐regulated in the kidneys from Gadd45β KO mice, whereas UUO‐mediated immune cell infiltration remained unchanged. The expression of pro‐inflammatory cytokines in response to LPS stimulation decreased in bone marrow‐derived macrophages from Gadd45β KO mice compared with that in WT mice. Importantly, UUO‐induced renal fibrosis was ameliorated in Gadd45β KO mice unlike in WT mice. Gadd45β was involved in TGF‐β signalling pathway regulation in kidney fibroblasts. Our findings demonstrate that Gadd45β plays a crucial role in renal injury and may be a therapeutic target for the treatment of CKD. |
| doi_str_mv | 10.1111/jcmm.15519 |
| format | Article |
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Here, we examined the effect of Gadd45β deletion on cell proliferation and apoptosis, inflammation, and renal fibrosis in an early chronic kidney disease (CKD) mouse model following unilateral ureteral obstruction (UUO). Wild‐type (WT) and Gadd45β‐knockout (KO) mice underwent either a sham operation or UUO and the kidneys were sampled eight days later. A histological assay revealed that ablation of Gadd45β ameliorated UUO‐induced renal injury. Cell proliferation was higher in Gadd45β KO mouse kidneys, but apoptosis was similar in both genotypes after UUO. Expression of pro‐inflammatory cytokines after UUO was down‐regulated in the kidneys from Gadd45β KO mice, whereas UUO‐mediated immune cell infiltration remained unchanged. The expression of pro‐inflammatory cytokines in response to LPS stimulation decreased in bone marrow‐derived macrophages from Gadd45β KO mice compared with that in WT mice. Importantly, UUO‐induced renal fibrosis was ameliorated in Gadd45β KO mice unlike in WT mice. Gadd45β was involved in TGF‐β signalling pathway regulation in kidney fibroblasts. Our findings demonstrate that Gadd45β plays a crucial role in renal injury and may be a therapeutic target for the treatment of CKD.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.15519</identifier><identifier>PMID: 32570293</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Ablation ; Animals ; Antibodies ; Antigens, Differentiation - genetics ; Antigens, Differentiation - metabolism ; Apoptosis ; Apoptosis - genetics ; Biomarkers ; Biopsy ; Bone marrow ; Cell cycle ; Cell growth ; Cell Line ; Cell Proliferation ; chronic kidney disease ; Clonal deletion ; Cytokines ; Cytokines - metabolism ; Disease Models, Animal ; Disease Susceptibility ; DNA damage ; Fibroblasts ; Fibrosis ; Gene Deletion ; Genes ; Genotypes ; Immunohistochemistry ; Inflammation ; Inflammation Mediators ; Kidney diseases ; Kidney Diseases - etiology ; Kidney Diseases - metabolism ; Kidney Diseases - pathology ; Kinases ; Laboratories ; Lipopolysaccharides ; Macrophages ; Male ; Mice ; Mice, Knockout ; Original ; Penicillin ; renal fibrosis ; Renal Insufficiency, Chronic - etiology ; Renal Insufficiency, Chronic - metabolism ; Renal Insufficiency, Chronic - pathology ; Signal transduction ; TGF‐β signalling ; Transforming Growth Factor beta - metabolism ; unilateral ureteral obstruction ; Ureteral Obstruction - complications</subject><ispartof>Journal of cellular and molecular medicine, 2020-08, Vol.24 (15), p.8814-8825</ispartof><rights>2020 The Authors. published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd</rights><rights>2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5469-62634741f618eec550cf4cb855f813396c5ca32e7ae6258dcf7c974229948d1f3</citedby><cites>FETCH-LOGICAL-c5469-62634741f618eec550cf4cb855f813396c5ca32e7ae6258dcf7c974229948d1f3</cites><orcidid>0000-0002-5779-6666</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7412396/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7412396/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,1411,11542,27903,27904,45553,45554,46031,46455,53770,53772</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32570293$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Moon, Sung‐Je</creatorcontrib><creatorcontrib>Kim, Jae‐Hoon</creatorcontrib><creatorcontrib>Choi, Young‐Keun</creatorcontrib><creatorcontrib>Lee, Chul‐Ho</creatorcontrib><creatorcontrib>Hwang, Jung Hwan</creatorcontrib><title>Ablation of Gadd45β ameliorates the inflammation and renal fibrosis caused by unilateral ureteral obstruction</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>The growth arrest and DNA damage‐inducible beta (Gadd45β) protein have been associated with various cellular functions, but its role in progressive renal disease is currently unknown. Here, we examined the effect of Gadd45β deletion on cell proliferation and apoptosis, inflammation, and renal fibrosis in an early chronic kidney disease (CKD) mouse model following unilateral ureteral obstruction (UUO). Wild‐type (WT) and Gadd45β‐knockout (KO) mice underwent either a sham operation or UUO and the kidneys were sampled eight days later. A histological assay revealed that ablation of Gadd45β ameliorated UUO‐induced renal injury. Cell proliferation was higher in Gadd45β KO mouse kidneys, but apoptosis was similar in both genotypes after UUO. Expression of pro‐inflammatory cytokines after UUO was down‐regulated in the kidneys from Gadd45β KO mice, whereas UUO‐mediated immune cell infiltration remained unchanged. The expression of pro‐inflammatory cytokines in response to LPS stimulation decreased in bone marrow‐derived macrophages from Gadd45β KO mice compared with that in WT mice. Importantly, UUO‐induced renal fibrosis was ameliorated in Gadd45β KO mice unlike in WT mice. Gadd45β was involved in TGF‐β signalling pathway regulation in kidney fibroblasts. Our findings demonstrate that Gadd45β plays a crucial role in renal injury and may be a therapeutic target for the treatment of CKD.</description><subject>Ablation</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Antigens, Differentiation - genetics</subject><subject>Antigens, Differentiation - metabolism</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Biomarkers</subject><subject>Biopsy</subject><subject>Bone marrow</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell Line</subject><subject>Cell Proliferation</subject><subject>chronic kidney disease</subject><subject>Clonal deletion</subject><subject>Cytokines</subject><subject>Cytokines - metabolism</subject><subject>Disease Models, Animal</subject><subject>Disease Susceptibility</subject><subject>DNA damage</subject><subject>Fibroblasts</subject><subject>Fibrosis</subject><subject>Gene Deletion</subject><subject>Genes</subject><subject>Genotypes</subject><subject>Immunohistochemistry</subject><subject>Inflammation</subject><subject>Inflammation Mediators</subject><subject>Kidney diseases</subject><subject>Kidney Diseases - etiology</subject><subject>Kidney Diseases - metabolism</subject><subject>Kidney Diseases - pathology</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Lipopolysaccharides</subject><subject>Macrophages</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Original</subject><subject>Penicillin</subject><subject>renal fibrosis</subject><subject>Renal Insufficiency, Chronic - etiology</subject><subject>Renal Insufficiency, Chronic - metabolism</subject><subject>Renal Insufficiency, Chronic - pathology</subject><subject>Signal transduction</subject><subject>TGF‐β signalling</subject><subject>Transforming Growth Factor beta - metabolism</subject><subject>unilateral ureteral obstruction</subject><subject>Ureteral Obstruction - complications</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kc9qFTEUxoMotlY3PoAE3Ihw6-TvJBuhXGpVWtzoOmQyJzaXmaQmM8p9LR-kz2TGuRZ10Wxy4PzynS_nQ-g5aU5JPW92bhxPiRBEP0DHRCi64Zrxh4eaKKaO0JNSdk3DJGH6MTpiVLQN1ewYxbNusFNIESePL2zfc3H7E9sRhpCynaDg6RpwiH6w47iCNvY4Q7QD9qHLqYSCnZ0L9Ljb4zmGqge5ducMa5G6MuXZLY-fokfeDgWeHe4T9OXd-eft-83lp4sP27PLjRNc6o2kkvGWEy-JAnBCNM5z1ykhvCKMaemEs4xCa0FSoXrnW6dbTqnWXPXEsxP0dtW9mbsRegdxqk7MTQ6jzXuTbDD_dmK4Nl_Td1OH0qpfBV4dBHL6NkOZzBiKg2GwEdJcDOVkMSmZrujL_9BdmnPdz0JJxZmiDbmfYo3mrLqv1OuVcnWxJYO_s0was4RtlrDN77Ar_OLvT96hf9KtAFmBH2GA_T1S5uP26moV_QW9JbXs</recordid><startdate>202008</startdate><enddate>202008</enddate><creator>Moon, Sung‐Je</creator><creator>Kim, Jae‐Hoon</creator><creator>Choi, Young‐Keun</creator><creator>Lee, Chul‐Ho</creator><creator>Hwang, Jung Hwan</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-5779-6666</orcidid></search><sort><creationdate>202008</creationdate><title>Ablation of Gadd45β ameliorates the inflammation and renal fibrosis caused by unilateral ureteral obstruction</title><author>Moon, Sung‐Je ; Kim, Jae‐Hoon ; Choi, Young‐Keun ; Lee, Chul‐Ho ; Hwang, Jung Hwan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5469-62634741f618eec550cf4cb855f813396c5ca32e7ae6258dcf7c974229948d1f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Ablation</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Antigens, Differentiation - genetics</topic><topic>Antigens, Differentiation - metabolism</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Biomarkers</topic><topic>Biopsy</topic><topic>Bone marrow</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell Line</topic><topic>Cell Proliferation</topic><topic>chronic kidney disease</topic><topic>Clonal deletion</topic><topic>Cytokines</topic><topic>Cytokines - metabolism</topic><topic>Disease Models, Animal</topic><topic>Disease Susceptibility</topic><topic>DNA damage</topic><topic>Fibroblasts</topic><topic>Fibrosis</topic><topic>Gene Deletion</topic><topic>Genes</topic><topic>Genotypes</topic><topic>Immunohistochemistry</topic><topic>Inflammation</topic><topic>Inflammation Mediators</topic><topic>Kidney diseases</topic><topic>Kidney Diseases - etiology</topic><topic>Kidney Diseases - metabolism</topic><topic>Kidney Diseases - pathology</topic><topic>Kinases</topic><topic>Laboratories</topic><topic>Lipopolysaccharides</topic><topic>Macrophages</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Original</topic><topic>Penicillin</topic><topic>renal fibrosis</topic><topic>Renal Insufficiency, Chronic - etiology</topic><topic>Renal Insufficiency, Chronic - metabolism</topic><topic>Renal Insufficiency, Chronic - pathology</topic><topic>Signal transduction</topic><topic>TGF‐β signalling</topic><topic>Transforming Growth Factor beta - metabolism</topic><topic>unilateral ureteral obstruction</topic><topic>Ureteral Obstruction - complications</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Moon, Sung‐Je</creatorcontrib><creatorcontrib>Kim, Jae‐Hoon</creatorcontrib><creatorcontrib>Choi, Young‐Keun</creatorcontrib><creatorcontrib>Lee, Chul‐Ho</creatorcontrib><creatorcontrib>Hwang, Jung Hwan</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>Wiley Free Content</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Moon, Sung‐Je</au><au>Kim, Jae‐Hoon</au><au>Choi, Young‐Keun</au><au>Lee, Chul‐Ho</au><au>Hwang, Jung Hwan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ablation of Gadd45β ameliorates the inflammation and renal fibrosis caused by unilateral ureteral obstruction</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2020-08</date><risdate>2020</risdate><volume>24</volume><issue>15</issue><spage>8814</spage><epage>8825</epage><pages>8814-8825</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>The growth arrest and DNA damage‐inducible beta (Gadd45β) protein have been associated with various cellular functions, but its role in progressive renal disease is currently unknown. Here, we examined the effect of Gadd45β deletion on cell proliferation and apoptosis, inflammation, and renal fibrosis in an early chronic kidney disease (CKD) mouse model following unilateral ureteral obstruction (UUO). Wild‐type (WT) and Gadd45β‐knockout (KO) mice underwent either a sham operation or UUO and the kidneys were sampled eight days later. A histological assay revealed that ablation of Gadd45β ameliorated UUO‐induced renal injury. Cell proliferation was higher in Gadd45β KO mouse kidneys, but apoptosis was similar in both genotypes after UUO. Expression of pro‐inflammatory cytokines after UUO was down‐regulated in the kidneys from Gadd45β KO mice, whereas UUO‐mediated immune cell infiltration remained unchanged. The expression of pro‐inflammatory cytokines in response to LPS stimulation decreased in bone marrow‐derived macrophages from Gadd45β KO mice compared with that in WT mice. Importantly, UUO‐induced renal fibrosis was ameliorated in Gadd45β KO mice unlike in WT mice. Gadd45β was involved in TGF‐β signalling pathway regulation in kidney fibroblasts. Our findings demonstrate that Gadd45β plays a crucial role in renal injury and may be a therapeutic target for the treatment of CKD.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>32570293</pmid><doi>10.1111/jcmm.15519</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-5779-6666</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Ablation Animals Antibodies Antigens, Differentiation - genetics Antigens, Differentiation - metabolism Apoptosis Apoptosis - genetics Biomarkers Biopsy Bone marrow Cell cycle Cell growth Cell Line Cell Proliferation chronic kidney disease Clonal deletion Cytokines Cytokines - metabolism Disease Models, Animal Disease Susceptibility DNA damage Fibroblasts Fibrosis Gene Deletion Genes Genotypes Immunohistochemistry Inflammation Inflammation Mediators Kidney diseases Kidney Diseases - etiology Kidney Diseases - metabolism Kidney Diseases - pathology Kinases Laboratories Lipopolysaccharides Macrophages Male Mice Mice, Knockout Original Penicillin renal fibrosis Renal Insufficiency, Chronic - etiology Renal Insufficiency, Chronic - metabolism Renal Insufficiency, Chronic - pathology Signal transduction TGF‐β signalling Transforming Growth Factor beta - metabolism unilateral ureteral obstruction Ureteral Obstruction - complications |
| title | Ablation of Gadd45β ameliorates the inflammation and renal fibrosis caused by unilateral ureteral obstruction |
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