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MicroRNA-22 increases senescence and activates cardiac fibroblasts in the aging heart

Please always quote using this URN: urn:nbn:de:bvb:20-opus-126745
  • MicroRNAs (miRs) are small non- coding RNA molecules controlling a plethora of biological processes such as development, cellular survival and senescence. We here determined miRs differentially regulated during cardiac postnatal development and aging. Cardiac function, morphology and miR expression profiles were determined in neonatal, 4 weeks, 6 months and 19 months old normotensive male healthy C57/Bl6N mice. MiR-22 was most prominently upregulated during cardiac aging. Cardiac expression of its bioinformatically predicted target mimecanMicroRNAs (miRs) are small non- coding RNA molecules controlling a plethora of biological processes such as development, cellular survival and senescence. We here determined miRs differentially regulated during cardiac postnatal development and aging. Cardiac function, morphology and miR expression profiles were determined in neonatal, 4 weeks, 6 months and 19 months old normotensive male healthy C57/Bl6N mice. MiR-22 was most prominently upregulated during cardiac aging. Cardiac expression of its bioinformatically predicted target mimecan (osteoglycin, OGN) was gradually decreased with advanced age. Luciferase reporter assays validated mimecan as a bona fide miR-22 target. Both, miR-22 and its target mimecan were co- expressed in cardiac fibroblasts and smooth muscle cells. Functionally, miR-22 overexpression induced cellular senescence and promoted migratory activity of cardiac fibroblasts. Small interference RNA-mediated silencing of mimecan in cardiac fibroblasts mimicked the miR-22-mediated effects. Rescue experiments revealed that the effects of miR-22 on cardiac fibroblasts were only partially mediated by mimecan. In conclusion, miR-22 upregulation in the aging heart contributed at least partly to accelerated cardiac fibroblast senescence and increased migratory activity. Our results suggest an involvement of miR-22 in age-associated cardiac changes, such as cardiac fibrosis.show moreshow less

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Metadaten
Author: Virginija Jazbutyte, Jan Fiedler, Susanne Kneitz, Paolo Galuppo, Annette Just, Angelika Holzmann, Johann Bauersachs, Thomas Thum
URN:urn:nbn:de:bvb:20-opus-126745
Document Type:Journal article
Faculties:Medizinische Fakultät / Theodor-Boveri-Institut für Biowissenschaften
Language:English
Parent Title (English):AGE
Year of Completion:2012
Volume:35
Issue:3
Pagenumber:747-762
Source:AGE (2013) 35:747–762 DOI 10.1007/s11357-012-9407-9
DOI:https://doi.org/10.1007/s11357-012-9407-9
Dewey Decimal Classification:6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit / 610 Medizin und Gesundheit
Tag:cardiac aging; cardiac fibrosis; miR-22; microRNAs; mimecan; osteoglycin
Release Date:2016/02/09
Licence (German):License LogoCC BY: Creative-Commons-Lizenz: Namensnennung