ArticleThe Journal of biological chemistry2012
Inhibition of cardiomyocytes differentiation of mouse embryonic stem cells by CD38/cADPR/Ca2+ signaling pathway.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- Targeting the SARM1-cADPR-CaArthritis research & therapy · 2026Article
- NADOxidative medicine and cellular longevity · 2023Review
- The Impact of Intermittent Hypoxia on Metabolism and Cognition.International journal of molecular sciences · 2022Review
- The phosphorylation and dephosphorylation switch of VCP/p97 regulates the architecture of centrosome and spindle.Cell death and differentiation · 2022Article
- Downregulation of the Cd38-Cyclic ADP-Ribose Signaling in Cardiomyocytes by Intermittent Hypoxia via Pten Upregulation.International journal of molecular sciences · 2022Article
- Article
- Intermittent Hypoxia Upregulates theInternational journal of molecular sciences · 2021Article
- Intracellular CaCell stem cell · 2019Article
- A multiscale analysis in CD38FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Specific cyclic ADP-ribose phosphohydrolase obtained by mutagenic engineering of MnScientific reports · 2018Article
- CD38 in the pathogenesis of allergic airway disease: Potential therapeutic targets.Pharmacology & therapeutics · 2017Review
- Mechanistic study of TRPM2-Ca(2+)-CAMK2-BECN1 signaling in oxidative stress-induced autophagy inhibition.Autophagy · 2016Article
- Contribution of Nrf2 to Atherogenic Phenotype Switching of Coronary Arterial Smooth Muscle Cells Lacking CD38 Gene.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2015Article
- Role of TRPV1 in the Differentiation of Mouse Embryonic Stem Cells into Cardiomyocytes.PloS one · 2015Article
- Roles and mechanisms of the CD38/cyclic adenosine diphosphate ribose/Ca(2+) signaling pathway.World journal of biological chemistry · 2014Review
- Two pore channel 2 (TPC2) inhibits autophagosomal-lysosomal fusion by alkalinizing lysosomal pH.The Journal of biological chemistry · 2013Article
- Two pore channel 2 differentially modulates neural differentiation of mouse embryonic stem cells.PloS one · 2013Article
- A cell permeable NPE caged ADP-ribose for studying TRPM2.PloS one · 2012Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cyclic adenosine diphosphoribose (cADPR) is an endogenous Ca(2+) mobilizing messenger that is formed by ADP-ribosyl cyclases from nicotinamide adenine dinucleotide (NAD). The main ADP-ribosyl cyclase in mammals is CD38, a multi-functional enzyme and a type II membrane protein. Here we explored the role of CD38-cADPR-Ca(2+) in the cardiomyogenesis of mouse embryonic stem (ES) cells. We found that the mouse ES cells are responsive to cADPR and possess the key components of the cADPR signaling pathway. In vitro cardiomyocyte (CM) differentiation of mouse ES cells was initiated by embryoid body (EB) formation. Interestingly, beating cells appeared earlier and were more abundant in CD38 knockdown EBs than in control EBs. Real-time RT-PCR and Western blot analyses further showed that the expression of several cardiac markers, including GATA4, MEF2C, NKX2.5, and α-MLC, were increased markedly in CD38 knockdown EBs than those in control EBs. Similarly, FACS analysis showed that more cardiac Troponin T-positive CMs existed in CD38 knockdown or 8-Br-cADPR, a cADPR antagonist, treated EBs compared with that in control EBs. On the other hand, overexpression of CD38 in mouse ES cells significantly inhibited CM differentiation. Moreover, CD38 knockdown ES cell-derived CMs possess the functional properties characteristic of normal ES cell-derived CMs. Last, we showed that the CD38-cADPR pathway negatively modulated the FGF4-Erks1/2 cascade during CM differentiation of ES cells, and transiently inhibition of Erk1/2 blocked the enhanced effects of CD38 knockdown on the differentiation of CM from ES cells. Taken together, our data indicate that the CD38-cADPR-Ca(2+) signaling pathway antagonizes the CM differentiation of mouse ES cells.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.