Inhibition of Cardiomyocytes Differentiation of Mouse Embryonic Stem Cells by CD38/cADPR/Ca2+ Signaling Pathway

Wei, Wenjie; Sun, Hai‐Ying; Ting, Kai Yiu; Zhang, Lihe; Lee, Hon Cheung; Li, Gui-Rong; Yue, Jianbo

doi:10.1074/jbc.m112.392530

Cited by 30 publications

(27 citation statements)

References 59 publications

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“…S2C). Similar results have also been observed in several other mouse ESC lines [14]. Taken together, these data suggest that CD38 is not essential for the pluripotency and self-renewal of mouse ESCs.…”

Section: Characterization Of the Cd38/cadpr/ca 21 Signaling In Esc-desupporting

confidence: 76%

“…Previously, we found that the expression of CD38 was increased during the differentiation of ESCs initiated by EB formation, and the final EB culture was a heterogenous mixture of various cell types and the proportion of neural lineage among them is low [14]. Interestingly, the expression of CD38 was markedly decreased during the differentiation of ESCs initiated by monolayer adherence culture (Fig.…”

Section: Characterization Of the Cd38/cadpr/ca 21 Signaling In Esc-dementioning

confidence: 99%

“…We have previously found that CD38 and ryanodine receptors were expressed in multiple mouse ESC lines, and these ESC lines were cADPR competent [14]. Here, we aimed to determine the role of this pathway in the neural differentiation of mouse ESC.…”

Section: Characterization Of the Cd38/cadpr/ca 21 Signaling In Esc-dementioning

confidence: 99%

“…Recently, we demonstrated that the CD38 signaling plays an important role in regulating cell proliferation and neuronal differentiation in PC12 cells [13], and the CD38 signaling also inhibits the cardiomyocyte differentiation of mouse ESCs [14]. Therefore, it is of interest to explore the involvement of the CD38 signaling in the neural differentiation of mouse ESCs.…”

Section: Introductionmentioning

confidence: 99%

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CD38 Is Required for Neural Differentiation of Mouse Embryonic Stem Cells by Modulating Reactive Oxygen Species

et al. 2015

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CD38 is a multifunctional membrane enzyme and the main mammalian ADP-ribosyl cyclase, which catalyzes the synthesis and hydrolysis of cADPR, a potent endogenous Ca 21 mobilizing messenger. Here, we explored the role of CD38 in the neural differentiation of mouse embryonic stem cells (ESCs). We found that the expression of CD38 was decreased during the differentiation of mouse ESCs initiated by adherent monoculture. Perturbing the CD38/cADPR signaling by either CD38 knockdown or treatment of cADPR antagonists inhibited the neural commitment of mouse ESCs, whereas overexpression of CD38 promoted it. Moreover, CD38 knockdown dampened reactive oxygen species (ROS) production during neural differentiation of ESCs by inhibiting NADPH oxidase activity, while CD38 overexpression enhanced it. Similarly, application of hydrogen peroxide mitigated the inhibitory effects of CD38 knockdown on neural differentiation of ESCs. Taken together, our data indicate that the CD38 signaling pathway is required for neural differentiation of mouse ESCs by modulating ROS production. STEM CELLS 2015; 33:2664-2673 SIGNIFICANCE STATEMENTThe in vitro generation of neural lineage cells from embryonic stem (ES) cells is a promising approach to produce cells suitable for neural tissue repair and cell-based replacement therapies of the nervous system. The functions regulated by the CD38 signaling are diverse. Here we found that the CD38 signaling pathway is required for neural differentiation of mouse ES cells by modulating ROS production. Our findings not only increase our understanding of ES cell differentiation and embryonic neural development, but also encourage the application of therapies based on ES cells in the treatment of neurological and psychiatric diseases.

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Section: Characterization Of the Cd38/cadpr/ca 21 Signaling In Esc-desupporting

confidence: 76%

Section: Characterization Of the Cd38/cadpr/ca 21 Signaling In Esc-dementioning

confidence: 99%

Section: Characterization Of the Cd38/cadpr/ca 21 Signaling In Esc-dementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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CD38 Is Required for Neural Differentiation of Mouse Embryonic Stem Cells by Modulating Reactive Oxygen Species

et al. 2015

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“…The synthesis and the hydrolysis of both NAADP and cADPR, are catalyzed by cluster of differentiation 38 (CD38) in mammalian cells. CD38 has also been detected in mouse D3, R1 and Sox1-GFP 46C ESCs [24] [25]. In addition to TRPC1 and TRPC2, other types of non-selective cation channels, such as TRPC3 and TRPC7 (unpublished This is the Pre-Published Version data) as well as transient receptor potential vanilloid 1 (TRPV1) [26] are also expressed in mouse Sox1-GFP 46C and D3 ESCs.…”

mentioning

confidence: 98%

The role of Ca2+ signaling on the self-renewal and neural differentiation of embryonic stem cells (ESCs)

et al. 2016

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Embryonic stem cells (ESCs) are promising resources for both scientific research and clinical regenerative medicine. With regards to the latter, ESCs are especially useful for treating several neurodegenerative disorders. Two significant characteristics of ESCs, which make them so valuable, are their capacity for self-renewal and their pluripotency, both of which are regulated by the integration of various signaling pathways. Intracellular Ca 2+ signaling is involved in several of these pathways. It is known to be precisely controlled by different Ca 2+ channels and pumps, which play an important role in a variety of cellular activities, including proliferation, differentiation and apoptosis. Here, we provide a review of the recent work conducted to investigate the function of Ca 2+ signaling in the self-renewal and the neural differentiation of ESCs. Specifically, we describe the role of intracellular Ca 2+ mobilization mediated by RyRs (ryanodine receptors); by cADPR (cyclic adenosine 5'-diphosphate ribose) and CD38 (cluster of differentiation 38/cADPR hydrolase); and by NAADP (nicotinic acid adenine dinucleotide phosphate) and TPC2 (two pore channel 2). We also discuss the Ca 2+ influx mediated by SOCs (store-operated Ca 2+ channels), TRPCs (transient receptor potential cation channels) and LTCC (L-type Ca 2+ channels) in the pluripotent ESCs as well as in neural differentiation of ESCs. Moreover, we describe the integration of Ca 2+ signaling in the other signaling pathways that are known to regulate the fate of ESCs.

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The protective effect of EGF‐activated ROS in human corneal epithelial cells by inducing mitochondrial autophagy via activation TRPM2

Huo

Chen

Zheng

et al. 2020

Journal Cellular Physiology

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Oxidative stress is a major pathogenesis of some ocular surface diseases. Our previous study demonstrated that epidermal growth factor (EGF)-activated reactive oxygen species (ROS) could protect against human corneal epithelial cell (HCE) injury. In the present study, we aimed to explore the role and mechanisms of oxidative stress and mitochondrial autophagy in HCE cells subjected to scratch injury. CCK-8 assays, EdU assays, Western blot analysis, wound-healing assays, and flow cytometry were conducted to determine cell viability, proliferation, protein expression, cell apoptosis, and intracellular ROS levels, respectively. The results showed that EGF could promote damage repair and inhibit cell apoptosis in scratch injured HCE cells by upregulating ROS (**p < .01, ***p < .001). EGF also induced mitochondrial autophagy and alleviated mitochondrial damage. Interestingly, the combination of the mitochondrial autophagy inhibitor and mitochondrial division inhibitor 1 (MDIVI-1) with EGF could reduce cell proliferation, viability, and the ROS level (*p < .05, **p < .01, ***p < .001). Treatment using the ROS inhibitor N-acetyl-L-cysteine abrogated the increase in mitochondrial membrane potential after EGF treatment. (*p < .05). Taken together, these findings indicated that EGF plays an important role in HCE damage repair and could activate ROS to protect against HCE injury by inducing mitochondrial autophagy via activation of TRPM2.

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Inhibition of Cardiomyocytes Differentiation of Mouse Embryonic Stem Cells by CD38/cADPR/Ca2+ Signaling Pathway

Cited by 30 publications

References 59 publications

CD38 Is Required for Neural Differentiation of Mouse Embryonic Stem Cells by Modulating Reactive Oxygen Species

CD38 Is Required for Neural Differentiation of Mouse Embryonic Stem Cells by Modulating Reactive Oxygen Species

The role of Ca2+ signaling on the self-renewal and neural differentiation of embryonic stem cells (ESCs)

The protective effect of EGF‐activated ROS in human corneal epithelial cells by inducing mitochondrial autophagy via activation TRPM2

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