Dataset Information

The role of Rpl3l in translation in cardiomyocytes

ABSTRACT: Ribosome immunoprecipitates of cardiomyocytes isolated from Rpl3l-/- and Rpl3l+/+ mouse hearts were analysed using mass spectrometry.

INSTRUMENT(S): LTQ Orbitrap Classic

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Heart, Regular Cardiac Myocyte

SUBMITTER: Eva Maria Novoa

LAB HEAD: Eva Maria Novoa Pardo

PROVIDER: PXD026985 | Pride | 2023-03-08

REPOSITORIES: Pride

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Publications

Dynamic interplay between RPL3- and RPL3L-containing ribosomes modulates mitochondrial activity in the mammalian heart.

Milenkovic Ivan I Santos Vieira Helaine Graziele HG Lucas Morghan C MC Ruiz-Orera Jorge J Patone Giannino G Kesteven Scott S Wu Jianxin J Feneley Michael M Espadas Guadalupe G Sabidó Eduard E Hübner Norbert N van Heesch Sebastiaan S Völkers Mirko M Novoa Eva Maria EM

Nucleic acids research 20230601 11

The existence of naturally occurring ribosome heterogeneity is now a well-acknowledged phenomenon. However, whether this heterogeneity leads to functionally diverse 'specialized ribosomes' is still a controversial topic. Here, we explore the biological function of RPL3L (uL3L), a ribosomal protein (RP) paralogue of RPL3 (uL3) that is exclusively expressed in skeletal muscle and heart tissues, by generating a viable homozygous Rpl3l knockout mouse strain. We identify a rescue mechanism in which, ...[more]

PMID: 36882085

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Project description:To compare expression profiles in the cardiomyocytes with wild type top2b and those with top2b deletion after in vivo treatment of mice with doxorubicin or drug vehicle Doxorubicin is widely used in modern cancer treatments, despite the advent of targeted therapy. However, a dose-dependent cardiotoxicity often limits its clinical use. The prevailing theory hypothesizes that doxorubicin-induced cardiotoxicity is the result of reactive oxygen species (ROS) generation due to redox-cycling of doxorubicin. Here we showed that cardiomyocyte-specific deletion of Topoisomerase II beta (Top2b) markedly reduced DNA double-strand breaks, apoptosis, and functional damages in doxorubicin-treated hearts. To investigate transcriptomic changes after doxorubicin treatment in wild type mouse and mouse with cardiac specific deletion of Top2b, we examined the expression profiles in 4 groups of mice (3/group), ie. wildtype mice with or without doxorubicin treatment and mice with Top2b deletion in the cardiomyocytes with or without doxorubicin treatment. Mice were treated with doxorubicin (25mg/kg, i.p.) or PBS (drug vehicle) for 16 hr or 72 hr. The heart was removed and cardiomyocytes were isolated by using a Langendorff apparatus. After purification, total RNA was extracted from the cardiomyocytes, purified, and used for gene expression analysis. Compared with that in control cardiomyocytes or cardiomyocytes with Top2b deletion, doxorubicin caused a significant expression change in the genome of cardiomyocytes from the wildtype mice. Among the changes, multiple genes encoding mitochondrial structural protein and components of the respiratory chain complexes were down-regulated 72 hr after treatment while multiple genes in the p53 pathway were up-regulated 16 hr after treatment in the wildtype cardiomyocytes. Expression changes were examined in 2 groups of mice (wild type and conditional knockout of top2b in the cardiomyocytes) treated with doxorubicin or PBS for 16 or 72 hours

Dataset Information

The role of Rpl3l in translation in cardiomyocytes

Publications

Dynamic interplay between RPL3- and RPL3L-containing ribosomes modulates mitochondrial activity in the mammalian heart.

Similar Datasets

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