miR-212 and miR-132 are required for epithelial stromal interactions necessary for mouse mammary gland development
Kamal Chowdhury and colleagues show that the microRNA-212/132 family is necessary for mouse mammary gland development. microRNA-212 and microRNA-132 are required in the mammary stroma, not the epithelium. MicroRNAs are small noncoding RNAs that carry out post-transcriptional regulation of the expres...
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| Veröffentlicht in: | Nature genetics 2010-12, Vol.42 (12), p.1101-1108 |
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| creator | Ucar, Ahmet Vafaizadeh, Vida Jarry, Hubertus Fiedler, Jan Klemmt, Petra A B Thum, Thomas Groner, Bernd Chowdhury, Kamal |
| description | Kamal Chowdhury and colleagues show that the microRNA-212/132 family is necessary for mouse mammary gland development. microRNA-212 and microRNA-132 are required in the mammary stroma, not the epithelium.
MicroRNAs are small noncoding RNAs that carry out post-transcriptional regulation of the expression of their target genes. However, their roles in mammalian organogenesis are only beginning to be understood. Here we show that the microRNA-212/132 family (which comprises miR-212 and miR-132) is indispensable during the development of the mammary glands in mice, particulary for the regulation of the outgrowth of the epithelial ducts. Mammary transplantation experiments revealed that the function of the miR-212/132 family is required in the stroma but not in the epithelia. Both miR-212 and miR-132 are expressed exclusively in mammary stroma and directly target the matrix metalloproteinase MMP-9. In glands that lack miR-212 and miR-132, MMP-9 expression increases and accumulates around the ducts. This may interfere with collagen deposition and lead to hyperactivation of the tumor growth factor-β signaling pathway, thereby impairing ductal outgrowth. Our results identify the miR-212/132 family as one of the main regulators of the epithelial-stromal interactions that are required for proper pubertal development of the mammary gland. |
| doi_str_mv | 10.1038/ng.709 |
| format | Article |
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MicroRNAs are small noncoding RNAs that carry out post-transcriptional regulation of the expression of their target genes. However, their roles in mammalian organogenesis are only beginning to be understood. Here we show that the microRNA-212/132 family (which comprises miR-212 and miR-132) is indispensable during the development of the mammary glands in mice, particulary for the regulation of the outgrowth of the epithelial ducts. Mammary transplantation experiments revealed that the function of the miR-212/132 family is required in the stroma but not in the epithelia. Both miR-212 and miR-132 are expressed exclusively in mammary stroma and directly target the matrix metalloproteinase MMP-9. In glands that lack miR-212 and miR-132, MMP-9 expression increases and accumulates around the ducts. This may interfere with collagen deposition and lead to hyperactivation of the tumor growth factor-β signaling pathway, thereby impairing ductal outgrowth. Our results identify the miR-212/132 family as one of the main regulators of the epithelial-stromal interactions that are required for proper pubertal development of the mammary gland.</description><identifier>ISSN: 1061-4036</identifier><identifier>EISSN: 1546-1718</identifier><identifier>DOI: 10.1038/ng.709</identifier><identifier>PMID: 21057503</identifier><identifier>CODEN: NGENEC</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>631/136/1660 ; 631/208/200 ; 631/337/384/331 ; 631/443/494 ; Agriculture ; Animal Genetics and Genomics ; Animals ; Biological and medical sciences ; Biomedical and Life Sciences ; Biomedicine ; Breast cancer ; Breasts ; Cancer Research ; Care and treatment ; Cell Communication ; Collagen ; Epithelial Cells - metabolism ; Epithelial Cells - pathology ; Female ; Fundamental and applied biological sciences. Psychology ; Gene Deletion ; Gene Expression Regulation, Developmental ; Gene Function ; Genes ; Genetic aspects ; Genetic regulation ; Genetics of eukaryotes. Biological and molecular evolution ; Human Genetics ; Mammary Glands, Animal - enzymology ; Mammary Glands, Animal - growth & development ; Mammary Glands, Animal - pathology ; Matrix Metalloproteinase 9 - metabolism ; Mice ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Molecular Sequence Data ; Mutation - genetics ; Physiological aspects ; Proteins ; Risk factors ; Rodents ; Signal Transduction ; Stromal Cells - metabolism ; Stromal Cells - pathology ; Transforming Growth Factor beta - metabolism</subject><ispartof>Nature genetics, 2010-12, Vol.42 (12), p.1101-1108</ispartof><rights>Springer Nature America, Inc. 2010</rights><rights>2015 INIST-CNRS</rights><rights>COPYRIGHT 2010 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Dec 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c632t-6a42415602c7a168a4055aeb5f4b6eb616154cc1b49527ccfc6e7ef307ec44f03</citedby><cites>FETCH-LOGICAL-c632t-6a42415602c7a168a4055aeb5f4b6eb616154cc1b49527ccfc6e7ef307ec44f03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/ng.709$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/ng.709$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23597349$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21057503$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ucar, Ahmet</creatorcontrib><creatorcontrib>Vafaizadeh, Vida</creatorcontrib><creatorcontrib>Jarry, Hubertus</creatorcontrib><creatorcontrib>Fiedler, Jan</creatorcontrib><creatorcontrib>Klemmt, Petra A B</creatorcontrib><creatorcontrib>Thum, Thomas</creatorcontrib><creatorcontrib>Groner, Bernd</creatorcontrib><creatorcontrib>Chowdhury, Kamal</creatorcontrib><title>miR-212 and miR-132 are required for epithelial stromal interactions necessary for mouse mammary gland development</title><title>Nature genetics</title><addtitle>Nat Genet</addtitle><addtitle>Nat Genet</addtitle><description>Kamal Chowdhury and colleagues show that the microRNA-212/132 family is necessary for mouse mammary gland development. microRNA-212 and microRNA-132 are required in the mammary stroma, not the epithelium.
MicroRNAs are small noncoding RNAs that carry out post-transcriptional regulation of the expression of their target genes. However, their roles in mammalian organogenesis are only beginning to be understood. Here we show that the microRNA-212/132 family (which comprises miR-212 and miR-132) is indispensable during the development of the mammary glands in mice, particulary for the regulation of the outgrowth of the epithelial ducts. Mammary transplantation experiments revealed that the function of the miR-212/132 family is required in the stroma but not in the epithelia. Both miR-212 and miR-132 are expressed exclusively in mammary stroma and directly target the matrix metalloproteinase MMP-9. In glands that lack miR-212 and miR-132, MMP-9 expression increases and accumulates around the ducts. This may interfere with collagen deposition and lead to hyperactivation of the tumor growth factor-β signaling pathway, thereby impairing ductal outgrowth. Our results identify the miR-212/132 family as one of the main regulators of the epithelial-stromal interactions that are required for proper pubertal development of the mammary gland.</description><subject>631/136/1660</subject><subject>631/208/200</subject><subject>631/337/384/331</subject><subject>631/443/494</subject><subject>Agriculture</subject><subject>Animal Genetics and Genomics</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Breast cancer</subject><subject>Breasts</subject><subject>Cancer Research</subject><subject>Care and treatment</subject><subject>Cell Communication</subject><subject>Collagen</subject><subject>Epithelial Cells - metabolism</subject><subject>Epithelial Cells - pathology</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. 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Kamal</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR-212 and miR-132 are required for epithelial stromal interactions necessary for mouse mammary gland development</atitle><jtitle>Nature genetics</jtitle><stitle>Nat Genet</stitle><addtitle>Nat Genet</addtitle><date>2010-12-01</date><risdate>2010</risdate><volume>42</volume><issue>12</issue><spage>1101</spage><epage>1108</epage><pages>1101-1108</pages><issn>1061-4036</issn><eissn>1546-1718</eissn><coden>NGENEC</coden><abstract>Kamal Chowdhury and colleagues show that the microRNA-212/132 family is necessary for mouse mammary gland development. microRNA-212 and microRNA-132 are required in the mammary stroma, not the epithelium.
MicroRNAs are small noncoding RNAs that carry out post-transcriptional regulation of the expression of their target genes. However, their roles in mammalian organogenesis are only beginning to be understood. Here we show that the microRNA-212/132 family (which comprises miR-212 and miR-132) is indispensable during the development of the mammary glands in mice, particulary for the regulation of the outgrowth of the epithelial ducts. Mammary transplantation experiments revealed that the function of the miR-212/132 family is required in the stroma but not in the epithelia. Both miR-212 and miR-132 are expressed exclusively in mammary stroma and directly target the matrix metalloproteinase MMP-9. In glands that lack miR-212 and miR-132, MMP-9 expression increases and accumulates around the ducts. This may interfere with collagen deposition and lead to hyperactivation of the tumor growth factor-β signaling pathway, thereby impairing ductal outgrowth. Our results identify the miR-212/132 family as one of the main regulators of the epithelial-stromal interactions that are required for proper pubertal development of the mammary gland.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>21057503</pmid><doi>10.1038/ng.709</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 631/136/1660 631/208/200 631/337/384/331 631/443/494 Agriculture Animal Genetics and Genomics Animals Biological and medical sciences Biomedical and Life Sciences Biomedicine Breast cancer Breasts Cancer Research Care and treatment Cell Communication Collagen Epithelial Cells - metabolism Epithelial Cells - pathology Female Fundamental and applied biological sciences. Psychology Gene Deletion Gene Expression Regulation, Developmental Gene Function Genes Genetic aspects Genetic regulation Genetics of eukaryotes. Biological and molecular evolution Human Genetics Mammary Glands, Animal - enzymology Mammary Glands, Animal - growth & development Mammary Glands, Animal - pathology Matrix Metalloproteinase 9 - metabolism Mice MicroRNAs - genetics MicroRNAs - metabolism Molecular Sequence Data Mutation - genetics Physiological aspects Proteins Risk factors Rodents Signal Transduction Stromal Cells - metabolism Stromal Cells - pathology Transforming Growth Factor beta - metabolism |
| title | miR-212 and miR-132 are required for epithelial stromal interactions necessary for mouse mammary gland development |
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