The RNA-binding protein Rbm38 is dispensable during pressure overload-induced cardiac remodeling in mice

• DOI: 10.1371/journal.pone.0184093
• Publication Date: 2017-08-29T13:38:52Z
• Authors: Maarten M. G. van...; Ingeborg van der ...; Abdelaziz Beqqali; Nina E. de Groot; Amin Damanafshan; Ralph J. van Oort; Yigal M. Pinto; Esther E. Creemers
• Keywords: Pressure overload

The importance of tightly controlled alternative pre-mRNA splicing in the heart is emerging. RNA binding protein Rbm24 has recently been identified as a pivotal cardiac splice factor, which governs sarcomerogenesis by controlling expression isoforms. Rbm38, homolog Rbm24, also implicated processes such splicing, stability and translation, but its function currently unknown. Here, we investigated role Rbm38 healthy diseased adult mouse heart. In contrast to heart- skeletal muscle-enriched appears be more broadly expressed. We generated somatic -/- mice show that global loss results hematopoietic defects. Specifically, were anemic displayed enlarged spleens with extramedullary hematopoiesis, shown earlier. hearts mildly hypertrophic, was not affected. Furthermore, deficiency did affect remodeling (i.e. hypertrophy, LV dilation fibrosis) or performance fractional shortening) after pressure-overload induced transverse aorta constriction. To further investigate molecular consequences deficiency, examined previously stability, translational targets Rbm38. found p21 HuR, Mef2d Fgfr2, translation target p53 altered, suggesting these are tissue-specific may counteracted redundancy mechanism. this regard, trend towards increased hearts. Overall, conclude critical does play