Altered expression of microRNA miR-146a correlates with the development of chronic renal inflammation
MicroRNAs (miRNAs) are highly conserved small non-coding RNAs that act as post-transcriptional regulators of target mRNA. In this study, we sought to identify the microRNA underlying local inflammation in a murine model of chronic kidney disease (CKD). In microarray analysis of kidneys, the expressi...
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| Veröffentlicht in: | Kidney international 2012-02, Vol.81 (3), p.280-292 |
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| creator | Ichii, Osamu Otsuka, Saori Sasaki, Nobuya Namiki, Yuka Hashimoto, Yoshiharu Kon, Yasuhiro |
| description | MicroRNAs (miRNAs) are highly conserved small non-coding RNAs that act as post-transcriptional regulators of target mRNA. In this study, we sought to identify the microRNA underlying local inflammation in a murine model of chronic kidney disease (CKD). In microarray analysis of kidneys, the expression of miR-146a/b was elevated in B6.MRLc1 CKD mice that spontaneously develop renal inflammation with age. Primary-microRNA analysis found that elevated miR-146a/b expression in the kidneys of B6.MRLc1 mice was mainly derived from miR-146a rather than miR-146b, and this expression increased with the development of CKD. Histopathological scores for glomerular and interstitial lesions, mRNA expression of inflammatory mediators, and macrophage infiltration were significantly higher in B6.MRLc1 than C57BL/6 mice and were positively correlated with miR-146a expression. In situ hybridization and laser microdissection–RT-PCR showed that miR-146a expression in interstitial lesions containing inflammatory cells was higher than in the glomerulus. The increased expression of the inflammatory-associated genes RELA, IRAK1, IL1B, IL10, and CXCLs was noted in miR-146a/b-silenced human monocytes. The amount of miR-146a was higher in urine sediments of B6.MRLc1 than of C57BL/6 mice. Thus, miR-146a expression in the kidneys and its urinary excretion was specifically associated with the development of interstitial lesions and correlated with inflammatory cell infiltration. |
| doi_str_mv | 10.1038/ki.2011.345 |
| format | Article |
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In this study, we sought to identify the microRNA underlying local inflammation in a murine model of chronic kidney disease (CKD). In microarray analysis of kidneys, the expression of miR-146a/b was elevated in B6.MRLc1 CKD mice that spontaneously develop renal inflammation with age. Primary-microRNA analysis found that elevated miR-146a/b expression in the kidneys of B6.MRLc1 mice was mainly derived from miR-146a rather than miR-146b, and this expression increased with the development of CKD. Histopathological scores for glomerular and interstitial lesions, mRNA expression of inflammatory mediators, and macrophage infiltration were significantly higher in B6.MRLc1 than C57BL/6 mice and were positively correlated with miR-146a expression. In situ hybridization and laser microdissection–RT-PCR showed that miR-146a expression in interstitial lesions containing inflammatory cells was higher than in the glomerulus. The increased expression of the inflammatory-associated genes RELA, IRAK1, IL1B, IL10, and CXCLs was noted in miR-146a/b-silenced human monocytes. The amount of miR-146a was higher in urine sediments of B6.MRLc1 than of C57BL/6 mice. Thus, miR-146a expression in the kidneys and its urinary excretion was specifically associated with the development of interstitial lesions and correlated with inflammatory cell infiltration.</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1038/ki.2011.345</identifier><identifier>PMID: 21975861</identifier><identifier>CODEN: KDYIA5</identifier><language>eng</language><publisher>Basingstoke: Elsevier Inc</publisher><subject>Animals ; Biological and medical sciences ; Chronic Disease ; chronic renal inflammation ; Female ; Inflammation Mediators - analysis ; interstitial lesion ; Kidney - pathology ; Medical sciences ; Mice ; Mice, Inbred C57BL ; microRNA ; MicroRNAs - physiology ; MicroRNAs - urine ; miR-146a ; monocyte/macrophage ; Monocytes - metabolism ; Nephritis - etiology ; Nephrology. Urinary tract diseases</subject><ispartof>Kidney international, 2012-02, Vol.81 (3), p.280-292</ispartof><rights>2012 International Society of Nephrology</rights><rights>2015 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Feb 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-9ceed99a6aed5a16a8a2580cfa323474ec079cb7e1fe610be50ea39880a80cf3</citedby><cites>FETCH-LOGICAL-c470t-9ceed99a6aed5a16a8a2580cfa323474ec079cb7e1fe610be50ea39880a80cf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25543349$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21975861$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ichii, Osamu</creatorcontrib><creatorcontrib>Otsuka, Saori</creatorcontrib><creatorcontrib>Sasaki, Nobuya</creatorcontrib><creatorcontrib>Namiki, Yuka</creatorcontrib><creatorcontrib>Hashimoto, Yoshiharu</creatorcontrib><creatorcontrib>Kon, Yasuhiro</creatorcontrib><title>Altered expression of microRNA miR-146a correlates with the development of chronic renal inflammation</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>MicroRNAs (miRNAs) are highly conserved small non-coding RNAs that act as post-transcriptional regulators of target mRNA. In this study, we sought to identify the microRNA underlying local inflammation in a murine model of chronic kidney disease (CKD). In microarray analysis of kidneys, the expression of miR-146a/b was elevated in B6.MRLc1 CKD mice that spontaneously develop renal inflammation with age. Primary-microRNA analysis found that elevated miR-146a/b expression in the kidneys of B6.MRLc1 mice was mainly derived from miR-146a rather than miR-146b, and this expression increased with the development of CKD. Histopathological scores for glomerular and interstitial lesions, mRNA expression of inflammatory mediators, and macrophage infiltration were significantly higher in B6.MRLc1 than C57BL/6 mice and were positively correlated with miR-146a expression. In situ hybridization and laser microdissection–RT-PCR showed that miR-146a expression in interstitial lesions containing inflammatory cells was higher than in the glomerulus. The increased expression of the inflammatory-associated genes RELA, IRAK1, IL1B, IL10, and CXCLs was noted in miR-146a/b-silenced human monocytes. The amount of miR-146a was higher in urine sediments of B6.MRLc1 than of C57BL/6 mice. Thus, miR-146a expression in the kidneys and its urinary excretion was specifically associated with the development of interstitial lesions and correlated with inflammatory cell infiltration.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Chronic Disease</subject><subject>chronic renal inflammation</subject><subject>Female</subject><subject>Inflammation Mediators - analysis</subject><subject>interstitial lesion</subject><subject>Kidney - pathology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>microRNA</subject><subject>MicroRNAs - physiology</subject><subject>MicroRNAs - urine</subject><subject>miR-146a</subject><subject>monocyte/macrophage</subject><subject>Monocytes - metabolism</subject><subject>Nephritis - etiology</subject><subject>Nephrology. 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Urinary tract diseases</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ichii, Osamu</creatorcontrib><creatorcontrib>Otsuka, Saori</creatorcontrib><creatorcontrib>Sasaki, Nobuya</creatorcontrib><creatorcontrib>Namiki, Yuka</creatorcontrib><creatorcontrib>Hashimoto, Yoshiharu</creatorcontrib><creatorcontrib>Kon, Yasuhiro</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Pascal-Francis</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>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma 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</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ichii, Osamu</au><au>Otsuka, Saori</au><au>Sasaki, Nobuya</au><au>Namiki, Yuka</au><au>Hashimoto, Yoshiharu</au><au>Kon, Yasuhiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Altered expression of microRNA miR-146a correlates with the development of chronic renal inflammation</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>2012-02-01</date><risdate>2012</risdate><volume>81</volume><issue>3</issue><spage>280</spage><epage>292</epage><pages>280-292</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><coden>KDYIA5</coden><abstract>MicroRNAs (miRNAs) are highly conserved small non-coding RNAs that act as post-transcriptional regulators of target mRNA. 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The increased expression of the inflammatory-associated genes RELA, IRAK1, IL1B, IL10, and CXCLs was noted in miR-146a/b-silenced human monocytes. The amount of miR-146a was higher in urine sediments of B6.MRLc1 than of C57BL/6 mice. Thus, miR-146a expression in the kidneys and its urinary excretion was specifically associated with the development of interstitial lesions and correlated with inflammatory cell infiltration.</abstract><cop>Basingstoke</cop><pub>Elsevier Inc</pub><pmid>21975861</pmid><doi>10.1038/ki.2011.345</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biological and medical sciences Chronic Disease chronic renal inflammation Female Inflammation Mediators - analysis interstitial lesion Kidney - pathology Medical sciences Mice Mice, Inbred C57BL microRNA MicroRNAs - physiology MicroRNAs - urine miR-146a monocyte/macrophage Monocytes - metabolism Nephritis - etiology Nephrology. Urinary tract diseases |
| title | Altered expression of microRNA miR-146a correlates with the development of chronic renal inflammation |
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