Dataset Information

Proteomic Analysis of the ubiquitination sites of KDM1A in rat myocardial tissue.

ABSTRACT: The ubiquitination sites of KDM1A in myocardial tissue were detected by Mass spectrometry.

INSTRUMENT(S):

ORGANISM(S): Rattus Norvegicus (rat)

TISSUE(S): Myocardium

DISEASE(S): Cardiovascular System Disease

SUBMITTER: Wan-Zhong Huang

LAB HEAD: Wan-Zhong Huang

PROVIDER: PXD070295 | Pride | 2026-01-19

REPOSITORIES: Pride

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Publications

USP16 S-nitrosylation aggravates coronary microembolization-induced myocardial injury via repressing KDM1A-mediated glutathione homeostasis.

Su Qiang Q Qin Jiao-Qin JQ Huang Yuan Y Dai Ri-Xin RX Wu Qing-Yun QY Mo Li-Rong LR Wu Qiang Q Huang Wan-Zhong WZ Yang Hua-Feng HF Liu Yang-Chun YC Pan Di-Guang DG

Nature communications 20251203 1

Coronary microembolization (CME) is a serious cardiovascular complication that causes severe cardiac dysfunction and arrhythmias. Glutathione (GSH) exhaustion-induced oxidative stress is a key contributor to CME. Here, we explore the molecular mechanisms underlying GSH imbalance during CME. We show that CME induces myocardial injury by disturbing GSH homeostasis, which is ameliorated by glutamate-cysteine ligase modifier subunit (GCLM) or glutaminase (GLS) overexpression. Lysine-specific histone ...[more]

PMID: 41339351

Similar Datasets

Project description:Background: The histone demethylase KDM1A is a multi-faceted regulator of critical developmental processes, including mesodermal and cardiac tube formation during mice gastrulation. The fine-tuning of KDM1A splicing has been linked to regulating the transcriptional program of excitable cells such as neurons. However, it is unknown whether modulating the expression of KDM1A isoforms is crucial for the specification and maintenance of cell identity of other cell types sensitive to electrical cues such as the cardiomyocytes. Objective: We investigated the role of ubKDM1A and KDM1A+2a ubiquitous splice variants during cardiomyogenesis and evaluated their impact on the regulation of cardiac differentiation in vitro. Methods and Results: We discovered a temporal modulation of ubKDM1A and KDM1A+2a isoform levels during human and mouse fetal cardiac development. Therefore, we generated human embryonic stem cells (hESCs) exclusively devoid of one or both isoforms and assessed their potential to derive cardiomyocytes. KDM1A depletion severely impaired cardiac differentiation. Conversely, KDM1A+2a-/- hESCs give rise to functional cardiomyocytes, displaying increased beating amplitude and frequency compared to wild-type cells. Transcriptomic profiling revealed that KDM1A-/- cardiomyocytes fail to activate an effective cardiac transcriptional program, while the depletion of KDM1A+2a enhances the expression of key cardiogenic markers. Notably, the impaired cardiac differentiation of KDM1A-/- cells can be rescued by re-expressing ubKDM1A or catalytically deficient ubKDM1A-K661A, but not by KDM1A+2a or KDM1A+2a-K661A. These data demonstrate a divergent role of the two KDM1A isoforms that is independent of their enzymatic activity. Through an exhaustive biochemical and genome-wide binding characterization, we excluded that the opposite ubKDM1A- and KDM1A+2a-mediated regulation of cardiac differentiation resides into differential substrate specificity, H3K4 demethylation efficiency, core-partners binding affinity, or alternative genome binding profiles. Conclusions: Our findings suggest the existence of a divergent scaffolding role of KDM1A splice variants during hESC differentiation into cardiomyocytes.

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