Overexpression of miR-30b in the developing mouse mammary gland causes a lactation defect and delays involution
MicroRNA (miRNA) are negative regulators of gene expression, capable of exerting pronounced influences upon the translation and stability of mRNA. They are potential regulators of normal mammary gland development and of the maintenance of mammary epithelial progenitor cells. This study was undertake...
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| Veröffentlicht in: | PloS one 2012-09, Vol.7 (9), p.e45727-e45727 |
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| creator | Le Guillou, Sandrine Sdassi, Nezha Laubier, Johann Passet, Bruno Vilotte, Marthe Castille, Johan Laloë, Denis Polyte, Jacqueline Bouet, Stéphan Jaffrézic, Florence Cribiu, Edmond-Paul Vilotte, Jean-Luc Le Provost, Fabienne |
| description | MicroRNA (miRNA) are negative regulators of gene expression, capable of exerting pronounced influences upon the translation and stability of mRNA. They are potential regulators of normal mammary gland development and of the maintenance of mammary epithelial progenitor cells. This study was undertaken to determine the role of miR-30b on the establishment of a functional mouse mammary gland. miR-30b is a member of the miR-30 family, composed of 6 miRNA that are highly conserved in vertebrates. It has been suggested to play a role in the differentiation of several cell types.
The expression of miR-30b was found to be regulated during mammary gland development. Transgenic mice overexpressing miR-30b in mammary epithelial cells were used to investigate its role. During lactation, mammary histological analysis of the transgenic mice showed a reduction in the size of alveolar lumen, a defect of the lipid droplets and a growth defect of pups fed by transgenic females. Moreover some mammary epithelial differentiated structures persisted during involution, suggesting a delay in the process. The genes whose expression was affected by the overexpression of miR-30b were characterized by microarray analysis.
Our data suggests that miR-30b is important for the biology of the mammary gland and demonstrates that the deregulation of only one miRNA could affect lactation and involution. |
| doi_str_mv | 10.1371/journal.pone.0045727 |
| format | Article |
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The expression of miR-30b was found to be regulated during mammary gland development. Transgenic mice overexpressing miR-30b in mammary epithelial cells were used to investigate its role. During lactation, mammary histological analysis of the transgenic mice showed a reduction in the size of alveolar lumen, a defect of the lipid droplets and a growth defect of pups fed by transgenic females. Moreover some mammary epithelial differentiated structures persisted during involution, suggesting a delay in the process. The genes whose expression was affected by the overexpression of miR-30b were characterized by microarray analysis.
Our data suggests that miR-30b is important for the biology of the mammary gland and demonstrates that the deregulation of only one miRNA could affect lactation and involution.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0045727</identifier><identifier>PMID: 23029204</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Agricultural sciences ; Alveoli ; Animals ; Apoptosis ; Base Sequence ; Biology ; Biopsy ; Breast cancer ; Breastfeeding & lactation ; Breasts ; Cell Differentiation ; Cells (biology) ; Deregulation ; DNA microarrays ; DNA Primers ; Epithelial cells ; Female ; Females ; Gene expression ; Lactation ; Lactation - genetics ; Life Sciences ; Mammary gland ; Mammary glands ; Mammary Glands, Animal - growth & development ; Mammary Glands, Animal - metabolism ; Metastasis ; Mice ; Mice, Transgenic ; MicroRNA ; MicroRNAs ; MicroRNAs - genetics ; miRNA ; mRNA stability ; Oligonucleotide Array Sequence Analysis ; Polymerase Chain Reaction ; Regulators ; Ribonucleic acid ; RNA ; Rodents ; Stem cells ; Transgenic animals ; Transgenic mice ; Vertebrates</subject><ispartof>PloS one, 2012-09, Vol.7 (9), p.e45727-e45727</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>Le Guillou et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><rights>2012 Le Guillou et al 2012 Le Guillou et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c687t-f9f2eb2a728d7fc5929f0069e81ddbe7ad4fe3708719a61d8afc8c79738d93f63</citedby><orcidid>0000-0001-8359-0760 ; 0000-0001-7579-6419 ; 0000-0003-4623-0584 ; 0000-0002-0588-5333 ; 0000-0002-0349-0047</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/PMC3454336/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3454336/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79569,79570</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23029204$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-01000363$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Le Guillou, Sandrine</creatorcontrib><creatorcontrib>Sdassi, Nezha</creatorcontrib><creatorcontrib>Laubier, Johann</creatorcontrib><creatorcontrib>Passet, Bruno</creatorcontrib><creatorcontrib>Vilotte, Marthe</creatorcontrib><creatorcontrib>Castille, Johan</creatorcontrib><creatorcontrib>Laloë, Denis</creatorcontrib><creatorcontrib>Polyte, Jacqueline</creatorcontrib><creatorcontrib>Bouet, Stéphan</creatorcontrib><creatorcontrib>Jaffrézic, Florence</creatorcontrib><creatorcontrib>Cribiu, Edmond-Paul</creatorcontrib><creatorcontrib>Vilotte, Jean-Luc</creatorcontrib><creatorcontrib>Le Provost, Fabienne</creatorcontrib><title>Overexpression of miR-30b in the developing mouse mammary gland causes a lactation defect and delays involution</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>MicroRNA (miRNA) are negative regulators of gene expression, capable of exerting pronounced influences upon the translation and stability of mRNA. They are potential regulators of normal mammary gland development and of the maintenance of mammary epithelial progenitor cells. This study was undertaken to determine the role of miR-30b on the establishment of a functional mouse mammary gland. miR-30b is a member of the miR-30 family, composed of 6 miRNA that are highly conserved in vertebrates. It has been suggested to play a role in the differentiation of several cell types.
The expression of miR-30b was found to be regulated during mammary gland development. Transgenic mice overexpressing miR-30b in mammary epithelial cells were used to investigate its role. During lactation, mammary histological analysis of the transgenic mice showed a reduction in the size of alveolar lumen, a defect of the lipid droplets and a growth defect of pups fed by transgenic females. Moreover some mammary epithelial differentiated structures persisted during involution, suggesting a delay in the process. The genes whose expression was affected by the overexpression of miR-30b were characterized by microarray analysis.
Our data suggests that miR-30b is important for the biology of the mammary gland and demonstrates that the deregulation of only one miRNA could affect lactation and involution.</description><subject>Agricultural sciences</subject><subject>Alveoli</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Base Sequence</subject><subject>Biology</subject><subject>Biopsy</subject><subject>Breast cancer</subject><subject>Breastfeeding & lactation</subject><subject>Breasts</subject><subject>Cell Differentiation</subject><subject>Cells (biology)</subject><subject>Deregulation</subject><subject>DNA microarrays</subject><subject>DNA Primers</subject><subject>Epithelial cells</subject><subject>Female</subject><subject>Females</subject><subject>Gene expression</subject><subject>Lactation</subject><subject>Lactation - genetics</subject><subject>Life Sciences</subject><subject>Mammary gland</subject><subject>Mammary glands</subject><subject>Mammary Glands, Animal - growth & 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of miR-30b in the developing mouse mammary gland causes a lactation defect and delays involution</title><author>Le Guillou, Sandrine ; Sdassi, Nezha ; Laubier, Johann ; Passet, Bruno ; Vilotte, Marthe ; Castille, Johan ; Laloë, Denis ; Polyte, Jacqueline ; Bouet, Stéphan ; Jaffrézic, Florence ; Cribiu, Edmond-Paul ; Vilotte, Jean-Luc ; Le Provost, Fabienne</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c687t-f9f2eb2a728d7fc5929f0069e81ddbe7ad4fe3708719a61d8afc8c79738d93f63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Agricultural sciences</topic><topic>Alveoli</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Base Sequence</topic><topic>Biology</topic><topic>Biopsy</topic><topic>Breast cancer</topic><topic>Breastfeeding & lactation</topic><topic>Breasts</topic><topic>Cell Differentiation</topic><topic>Cells 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Fabienne</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Overexpression of miR-30b in the developing mouse mammary gland causes a lactation defect and delays involution</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2012-09-24</date><risdate>2012</risdate><volume>7</volume><issue>9</issue><spage>e45727</spage><epage>e45727</epage><pages>e45727-e45727</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>MicroRNA (miRNA) are negative regulators of gene expression, capable of exerting pronounced influences upon the translation and stability of mRNA. They are potential regulators of normal mammary gland development and of the maintenance of mammary epithelial progenitor cells. This study was undertaken to determine the role of miR-30b on the establishment of a functional mouse mammary gland. miR-30b is a member of the miR-30 family, composed of 6 miRNA that are highly conserved in vertebrates. It has been suggested to play a role in the differentiation of several cell types.
The expression of miR-30b was found to be regulated during mammary gland development. Transgenic mice overexpressing miR-30b in mammary epithelial cells were used to investigate its role. During lactation, mammary histological analysis of the transgenic mice showed a reduction in the size of alveolar lumen, a defect of the lipid droplets and a growth defect of pups fed by transgenic females. Moreover some mammary epithelial differentiated structures persisted during involution, suggesting a delay in the process. The genes whose expression was affected by the overexpression of miR-30b were characterized by microarray analysis.
Our data suggests that miR-30b is important for the biology of the mammary gland and demonstrates that the deregulation of only one miRNA could affect lactation and involution.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23029204</pmid><doi>10.1371/journal.pone.0045727</doi><tpages>e45727</tpages><orcidid>https://orcid.org/0000-0001-8359-0760</orcidid><orcidid>https://orcid.org/0000-0001-7579-6419</orcidid><orcidid>https://orcid.org/0000-0003-4623-0584</orcidid><orcidid>https://orcid.org/0000-0002-0588-5333</orcidid><orcidid>https://orcid.org/0000-0002-0349-0047</orcidid><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_plos_journals_1326550901 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Agricultural sciences Alveoli Animals Apoptosis Base Sequence Biology Biopsy Breast cancer Breastfeeding & lactation Breasts Cell Differentiation Cells (biology) Deregulation DNA microarrays DNA Primers Epithelial cells Female Females Gene expression Lactation Lactation - genetics Life Sciences Mammary gland Mammary glands Mammary Glands, Animal - growth & development Mammary Glands, Animal - metabolism Metastasis Mice Mice, Transgenic MicroRNA MicroRNAs MicroRNAs - genetics miRNA mRNA stability Oligonucleotide Array Sequence Analysis Polymerase Chain Reaction Regulators Ribonucleic acid RNA Rodents Stem cells Transgenic animals Transgenic mice Vertebrates |
| title | Overexpression of miR-30b in the developing mouse mammary gland causes a lactation defect and delays involution |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-16T10%3A00%3A25IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Overexpression%20of%20miR-30b%20in%20the%20developing%20mouse%20mammary%20gland%20causes%20a%20lactation%20defect%20and%20delays%20involution&rft.jtitle=PloS%20one&rft.au=Le%20Guillou,%20Sandrine&rft.date=2012-09-24&rft.volume=7&rft.issue=9&rft.spage=e45727&rft.epage=e45727&rft.pages=e45727-e45727&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0045727&rft_dat=%3Cgale_plos_%3EA498252048%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1326550901&rft_id=info:pmid/23029204&rft_galeid=A498252048&rft_doaj_id=oai_doaj_org_article_13d4caa906d94b088fcb3d2a57fc3103&rfr_iscdi=true |