Dataset Information

Characterisation of directed maturation in human cardiac organoids

ABSTRACT: Cardiac maturation is an important developmental phase where there are profound biological and functional changes after birth in mammals. Herein, we use our profiling of human heart maturation in vivo to identify key drivers of maturation in our human cardiac organoid (hCO) model. After screening of various metabolism modulating factors, we established a directed maturation (DM) protocol to induce mature cardiac expression and compared the proteomic changes to our original serum free (SF) protocol. In this dataset, we compared 4 replicates of DM to 4 replicates of SF derived cardiac organoids using global DIA-MS/MS.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Heart, Cell Culture, Embryonic Stem Cell

DISEASE(S): Cardiovascular System Disease

SUBMITTER: Harley Robinson

LAB HEAD: Prof James Hudson

PROVIDER: PXD059940 | Pride | 2025-04-17

REPOSITORIES: Pride

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Publications

Maturation of human cardiac organoids enables complex disease modeling and drug discovery.

Pocock Mark W MW Reid Janice D JD Robinson Harley R HR Charitakis Natalie N Krycer James R JR Foster Simon R SR Fitzsimmons Rebecca L RL Lor Mary M Devilée Lynn A C LAC Batho Christopher A P CAP Tuano Natasha N Howden Sara E SE Vlahos Katerina K Watt Kevin I KI Piers Adam T AT Bibby Kaitlyn K McNamara James W JW Sutton Rebecca R Iaprintsev Valerii V Mathew Jacob J Voges Holly K HK Fortuna Patrick R J PRJ Bass-Stringer Sebastian S Vivien Celine C Rae James J Parton Robert G RG Firulli Anthony B AB Lisowski Leszek L Huckstep Hannah H Humphrey Sean J SJ Lal Sean S Konstantinov Igor E IE Weintraub Robert G RG Elliott David A DA Ramialison Mirana M Porrello Enzo R ER Mills Richard J RJ Hudson James E JE

Nature cardiovascular research 20250625 7

Maturation of human pluripotent stem (hPS) cell-derived cardiomyocytes is critical for their use as a model system. Here we mimic human heart maturation pathways in the setting of hPS cell-derived cardiac organoids (hCOs). Specifically, transient activation of 5' AMP-activated protein kinase and estrogen-related receptor enhanced cardiomyocyte maturation, inducing expression of mature sarcomeric and oxidative phosphorylation proteins, and increasing metabolic capacity. hCOs generated using the d ...[more]

PMID: 40562874

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Project description:Background: Sustained sleep insufficiency impairs immune system and increases the adverse outcomes of cardiovascular diseases. However, the role and mechanisms prolonged sleep fragmentation (SF) on the outcomes of myocardial infarction (MI) remains elusive. Methods: Among 497 MI patients with complete sleep data participating in the National Health and Nutrition Examination Survey, the association between different types of sleep disorders and post-MI survivability was evaluated. We then developed a mouse model with 10 weeks of SF followed by MI surgery. Emergency hematopoiesis and neutrophil expansion were analyzed. Potential mechanisms were explored using bone marrow (BM) transplantation, anti-SiglecF neutralizing antibodies and Interferon alpha and beta receptor subunit 1 knockout (Ifnar1-/-) in BM. Results: Frequent nocturnal awakening independently predicted reduced survival rate of MI patients, with a hazard ratio (HR) of 2.136 (95% CI=1.142-3.995). Increased infarct size, deteriorated cardiac function and lower survival rate were also observed in MI mice pretreated with 10-week SF. SF facilitated post-MI neutrophil expansion and infiltration into infarct area, differentiating into SiglecFhi subset. Inhibition of SiglecFhi neutrophils allowed for the alleviations of post-MI cardiac remodeling. Furthermore, BM progenitors were skewed toward neutrophil lineage concomitant with the clonal expansion of granulocyte-monocyte progenitors (GMPs) in MI mice pretreated with 10-week SF. Transcriptome analysis and functional experiments revealed that activation of type I interferon (IFN) signaling was involved in this process, while depletion of Ifnar1 in BM and administration of IFNAR1-neutralizing antibodies significantly alleviated post-MI cardiac remodeling and neutrophil expansion. Conclusions: SF aggravates post-MI cardiac remodeling and dysfunction through promoting GMP differentiation and neutrophil expansion. Blockage of type I IFN could alleviate this detrimental influence.

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	20241206_DM_1.raw	Raw
	20241206_DM_2.raw	Raw
	20241206_DM_3.raw	Raw
	20241206_DM_4.raw	Raw
	20241206_SF_1.raw	Raw