Dataset Information

Pro-regenerative fingerprints identified in a sub-population of adult mouse cardiomyocytes by integrative single-cell proteomics-Analytical dataset

ABSTRACT: We present a new experimental and computational workflow to analyze single-cell proteomics data applied to single-cardiomyocytes. By using an optimized isolation procedure and by taking advantage of the integrative capabilities of iSanXoT application, we eliminate batch effects, minimize cell size-related biases, obtain quantitative subcellular compartment information and detect protein alterations within subcellular compartments. This approach enhances data quantification accuracy and facilitates biological interpretation. We show that the overexpression of the Myc transcription factor switches the metabolism of adult cardiomyocytes and establishes a subpopulation of pro-regenerative cardiomyocytes. The reported advances pave the way for systematic analysis of single-cell proteomes, including those of sensitive cells, like cardiomyocytes.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Heart, Cardiac Muscle Cell

SUBMITTER: Consuelo Marín-Vicente

LAB HEAD: Jesús Vázquez

PROVIDER: PXD064518 | Pride | 2026-04-06

REPOSITORIES: Pride

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	20221018_Ec_02_SC_CNIC-KI_TMT1.mzML	Mzml
	20221018_Ec_02_SC_CNIC-KI_TMT1.mzid	Mzid
	20221018_Ec_02_SC_CNIC-KI_TMT1.raw	Raw
	20221019_Ec_01_SC_CNIC-KI_TMT12.mzML	Mzml
	20221019_Ec_01_SC_CNIC-KI_TMT12.mzid	Mzid

Items per page:

1 - 5 of 243

Similar Datasets

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

Pro-regenerative fingerprints identified in a sub-population of adult mouse cardiomyocytes by integrative single-cell proteomics-Analytical dataset

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets