ArticleJournal of molecular and cellular cardiology2016
Mesenchymal stem cells suppress cardiac alternans by activation of PI3K mediated nitroso-redox pathway.
Article in Journal of molecular and cellular cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Advances in stem cell therapy for erectile dysfunction: preclinical evidence and emerging therapeutic approaches.Frontiers in medicine · 2025Review
- Nonmyocytes as electrophysiological contributors to cardiac excitation and conduction.American journal of physiology. Heart and circulatory physiology · 2023Review
- Stem Cell Therapy for Erectile Dysfunction: A Step towards a Future Treatment.Life (Basel, Switzerland) · 2023Review
- Adipogenic Signaling Promotes Arrhythmia Substrates before Structural Abnormalities in TMEM43 ARVC.Journal of personalized medicine · 2022Article
- Elucidating arrhythmogenic right ventricular cardiomyopathy with stem cells.Birth defects research · 2022Review
- Human Cardiac Mesenchymal Stem Cells Remodel in Disease and Can Regulate Arrhythmia Substrates.Circulation. Arrhythmia and electrophysiology · 2020Article
- Physiologic, Pathologic, and Therapeutic Paracrine Modulation of Cardiac Excitation-Contraction Coupling.Circulation research · 2018Review
- How Do Mesenchymal Stem Cells Influence or Are Influenced by Microenvironment through Extracellular Vesicles Communication?Frontiers in cell and developmental biology · 2017Review
- An infrared optical pacing system for screening cardiac electrophysiology in human cardiomyocytes.PloS one · 2017Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe paracrine action of non-cardiac progenitor cells is robust, but not well understood. Mesenchymal stem cells (MSC) have been shown to enhance calcium (Ca(++)) cycling in myocytes. Therefore, we hypothesized that MSCs can suppress cardiac alternans, an important arrhythmia substrate, by paracrine action on Ca(++) cycling. METHODS AND
resultsHuman cardiac myocyte monolayers derived from iPS cells (hCM) were cultured without or with human MSCs (hMSC) directly or plated on a transwell insert. Ca(++) transient alternans (Ca(++) ALT) and Ca(++) transient duration (CaD) were measured from hCM monolayers following application of 200μM H2O2. Ca(++) ALT in hCM was significantly decreased when cultured with hMSCs directly (97%, p<0.0001) and when cultured with hMSC in the transwell insert (80%, p<0.0001). When hCM with hMSCs were pretreated with PI3K or eNOS inhibitors, Ca(++) ALT was larger than baseline by 20% (p<0.0001) and 36% (p<0.0001), respectively. In contrast, Ca(++) ALT was reduced by 89% compared to baseline (p<0.0001) when hCM monolayers without hMSCs were pretreated with 20μM GSNO. In all experiments, changes in Ca(++) ALT were mirrored by changes in CaD. Finally, real time quantitative PCR revealed no significant differences in mRNA expression of RyR2, SERCA2a, and phospholamban between hCM cultured with or without hMSCs.
conclusionCa(++) ALT is suppressed by hMSCs in a paracrine fashion due to activation of a PI3K-mediated nitroso-redox pathway. These findings demonstrate, for the first time, how stem cell therapy might be antiarrhythmic by suppressing cardiac alternans through paracrine action on Ca(++) cycling.
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