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          Institute: MPI für Herz- und Lungenforschung (W. G. Kerckhoff Institut)     Collection: Yearbook 2016     Display Documents



  history
ID: 723925.0, MPI für Herz- und Lungenforschung (W. G. Kerckhoff Institut) / Yearbook 2016
Generation and Validation of miR-142 Knock Out Mice
Authors:Shrestha, A.; Carraro, G.; El Agha, E.; Mukhametshina, R.; Chao, C. M.; Rizvanov, A.; Barreto, G.; Bellusci, S.
Date of Publication (YYYY-MM-DD):2015
Title of Journal:PLoS ONE
Volume:10
Issue / Number:9
Start Page:e0136913
Audience:Not Specified
Abstract / Description:microRNA-142 (miR-142) is an important regulator of many biological processes and associated signaling pathways during embryonic development, homeostasis and disease. The miR-142 hairpin gives rise to the "guide strand" miR-142-3p and the sister "passenger" strand miR-142-5p. miR-142-3p has been shown to play critical, non-redundant functions in the development of the hematopoietic lineage. We have recently reported that miR-142-3p is critical for the control of Wnt signaling in the mesenchyme of the developing lung. miR-142-5p has been proposed to control adaptive growth in cardiomyocytes postnatally and its increase is associated with extensive apoptosis and cardiac dysfunction in a murine heart failure model. Using homologous recombination, we now report the generation and validation of miR-142-null mice. miR-142-null mice show a significant decrease in th expression levels of both the 3p and 5p isoforms. The expression of Bzrap1, a gene immediately flanking miR-142 is not altered while the expression of a long non-coding RNA embedded within the miR-142 gene is decreased. miR-142-null newborn pups appear normal and are normally represented indicating absence of embryonic lethality. At embryonic day 18.5, miR-142-null lungs display increased Wnt signaling associated with the up-regulation of Apc and p300, two previously reported targets of miR-142-3p and -5p, respectively. Adult miR-142-null animals display impaired hematopoietic lineage formation identical to previously reported miR-142 gene trap knockdown mice. We report, for the first time, the homologous recombination-based miR-142-null mice that will be useful for the scientific community working on the diverse biological functions of miR-142.
External Publication Status:published
Document Type:Article
Version Comment:Automatic journal name synchronization
Communicated by:n.n.
Affiliations:MPI für physiologische und klinische Forschung
External Affiliations:Lung and Regenerative Medicine Institutes, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California. Institute of Fundamental Medicine and Biology, Kazan (Volga Region) Federal University, Kazan, Russian Federation. LOEWE Research Group Lung Cancer Epigenetic Max Plank Institute, Bad Nauheim, Germany; Member of the German Center for Lung Research, Giessen, Germany. German Center for Lung Research, Excellence Cluster Cardio-Pulmonary System, Universities of Giessen and Marburg Lung Center, Giessen, Hessen, Germany; Institute of Fundamental Medicine and Biology, Kazan (Volga Region) Federal University, Kazan, Russian Federation; Member of the German Center for Lung Research, Giessen, Germany; Developmental Biology Program, Division of Surgery, Saban Research Institute of Children's Hospital Los Angeles, University of Southern California Keck School of Medicine, Los Angeles, California.
Identifiers:ISSN:1932-6203 (Electronic) 1932-6203 (Linking) %R 10.1371/journal.pone.0136913
URL:http://www.ncbi.nlm.nih.gov/pubmed/26327117
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