<i>Notch1</i>Signaling Antagonizes Transforming Growth Factor-β Pathway and Induces Apoptosis in Rabbit Trophoblast Stem Cells

Tan, Tao; Lü, Bin; Zhang, Jing; Niu, Yuyu; Si, Wei; Wei, Qiang; Ji, Weizhi

doi:10.1089/scd.2013.0280

Cited by 8 publications

(3 citation statements)

References 37 publications

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“…Notch signaling is involved in the maintenance of neural progenitors in an undifferentiated state, in part by inhibition of neurogenesis, and it influences synaptic plasticity, learning, and memory in the adult brain. 19,22 NICD translocates to the nucleus where it functions as a transcriptional coactivator in conjunction with the CBF-1/Su(H)/LAG-1 (CSL) family of DNA-binding proteins by recruiting general transcription factors, including CBP/p300. [23][24][25] NICD-mediated transcription induces expression of genes such as Hairy-Enhancer of Split (Hes) and Hes-related protein (Herp).…”

Section: Discussionmentioning

confidence: 99%

Interplay between Notch and p53 promotes neuronal cell death in ischemic stroke

Balaganapathy

Baik

Mallilankaraman

et al. 2017

J Cereb Blood Flow Metab

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Stroke is the world's second leading cause of mortality, with a high incidence of morbidity. Numerous neuronal membrane receptors are activated by endogenous ligands and may contribute to infarct development. Notch is a well-characterized membrane receptor involved in cell differentiation and proliferation, and now shown to play a pivotal role in cell death during ischemic stroke. Blockade of Notch signaling by inhibition of γ-secretase, an enzyme that generates the active form of Notch, is neuroprotective following stroke. We have also identified that Pin1, a peptidyl-prolyl isomerase that regulates p53 transactivation under stress, promotes the pathogenesis of ischemic stroke via Notch signaling. Moreover, Notch can also mediate cell death through a p53-dependent pathway, resulting in apoptosis of neural progenitor cells. The current study has investigated the interplay between Notch and p53 under ischemic stroke conditions. Using pharmacological inhibitors, we have demonstrated that a Notch intracellular domain (NICD)/p53 interaction is involved in transcriptional regulation of genes downstream of p53 and NICD to modify stroke severity. Furthermore, the NICD/p53 interaction confers stability to p53 by rescuing it from ubiquitination. Together, these results indicate that Notch contributes to the pathogenesis of ischemic stroke by promoting p53 stability and signaling.

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Section: Discussionmentioning

confidence: 99%

Interplay between Notch and p53 promotes neuronal cell death in ischemic stroke

Balaganapathy

Baik

Mallilankaraman

et al. 2017

J Cereb Blood Flow Metab

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“…Many factors are involved in apoptosis process, such as Fas, Fas ligand (Fas-L), caspase-8, Bcl-2 family, Mcl-1、p53 26 . There are few reports on the effect of Notch signaling pathway on apoptosis of cytotrophoblasts 27 , and there is no study about the role of Notch2 and Notch3 in apoptosis of cytotrophoblasts till now. Notch2 and Notch3 which are mainly expressed in villous cytotrophoblast cells 5 can regulate proliferation of BeWo and JAR cells in the present paper, and since villous trophoblasts are kept in a steady state with the relative amounts of cytotrophoblast and syncytiotrophoblast 14 , 15 , we hypothesize that Notch2 and Notch3 may take part in cytotrophoblast apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Effects of Notch2 and Notch3 on Cell Proliferation and Apoptosis of Trophoblast Cell Lines

Zhao¹,

Zhuang²,

Huang³

et al. 2015

Int. J. Med. Sci.

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Aims: To investigate the effect of Notch2 and Notch3 on cell proliferation and apoptosis of two trophoblast cell lines, BeWo and JAR.Methods: Notch2 and Notch3 expression in BeWo and JAR cells was upregulated or downregulated using lentivirus-mediated overexpression or RNA interference. The effect of Notch2 and Notch3 on cell proliferation was assessed by the CCK-8 assay. The effect of Notch2 and Notch3 on the apoptosis of BeWo and JAR cells was evaluated by flow cytometry using the Annexin V-PE Apoptosis kit. Lentivirus-based overexpression vectors were constructed by cloning the full-length coding sequences of human Notch2 and Notch3 C-terminally tagged with GFP or GFP alone (control) into a lentivirus-based expression vector. Lentivirus-based gene silencing vectors were prepared by cloning small interfering sequences targeting human Notch2 and Notch3 and scrambled control RNA sequence into a lentivirus-based gene knockdown vector. The effect of Notch2 and Notch3 on cell proliferation was assessed by the CCK-8 assay. And the effect of Notch2 and Notch3 on the apoptosis of BeWo and JAR cells was evaluated by flow cytometry using the Annexin V PE Apoptosis kit.Results: We found that the downregulation of Notch2 and Notch3 gene expression in BeWo and JAR cells resulted in an increase in cell proliferation, while upregulation of Notch3 and Notch2 expression led to a decrease in cell proliferation. Moreover, the overexpression of Notch3 and Notch2 in BeWo and JAR cells reduced apoptosis in these trophoblast cell lines, whereas apoptosis was increased in the cells in which the expression of Notch3 and Notch2 was downregulated.Conclusions: Notch2 and Notch3 inhibited both cell proliferation and cell apoptosis in BeWo and JAR trophoblast cell lines.

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“…Following nuclear translocation, NICD forms a complex with the recombination signal binding protein for immunoglobulin kappa J region (also known as CSL) to regulate the transcription of Notch target genes, such as Hes1 and Hes5 . Many researchers have found that Notch signaling can interfere with apoptosis of lymphocytes, tumor cells, and stem cells by regulating caspase-dependent or -independent pathways. − Notch pathway activation exacerbates the apoptotic neuron in the dentate gyrus of rats in a post-stroke depressive symptom model . Bailis et al demonstrated that the Notch pathway can directly regulate the differentiation of Th1 and Th2 subsets, thus affecting the immune state of the body .…”

Section: Introductionmentioning

confidence: 99%

Lycopene Alleviates Chronic Stress-Induced Spleen Apoptosis and Immunosuppression via Inhibiting the Notch Signaling Pathway in Rats

Zhang

Zhao

Sun

et al. 2022

J. Agric. Food Chem.

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Chronic stress induction in immunosuppression and splenocyte apoptosis is commonly associated with increased susceptibility to various diseases. Lycopene (LYC) is a member of the carotenoid family with immune restoration and anti-apoptotic function. However, little is known about the mechanisms underlying the protective roles of LYC against spleen injury induced by chronic stress. Herein, male Wistar rats were undergoing chronic restraint stress and/or administered LYC (10 mg/kg) for 21 days. The effective model establishment was validated by open-field tests and levels of corticosterone in serum. Histopathological staining observation displayed that LYC could reduce chronic stress-induced spleen structure damage. Furthermore, LYC treatment significantly reduced the number of apoptotic-positive splenocytes caused by chronic stress via the death receptor apoptotic pathway. We detected the interleukin 4 and interferon γ levels in serum and spleen to determine the ratio of Th1 and Th2 and found that LYC can alleviate the immunosuppression induced by chronic stress. Notably, western blot and real-time polymerase chain reaction indicated that LYC can reduce the expression of the Notch-pathway-related proteins and mRNA in rats exposed to chronic stress. Further study of the potential mechanisms by adding the Notch pathway inhibitor DAPT revealed that LYC alleviates the structure damage, apoptosis, and immunosuppression caused by chronic stress via the suppression of the Notch pathway. Overall, this study presents a strong rationale to target LYC as a treatment strategy to relieve chronic stress-induced spleen injury.

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Notch1Signaling Antagonizes Transforming Growth Factor-β Pathway and Induces Apoptosis in Rabbit Trophoblast Stem Cells

Cited by 8 publications

References 37 publications

Interplay between Notch and p53 promotes neuronal cell death in ischemic stroke

Interplay between Notch and p53 promotes neuronal cell death in ischemic stroke

Effects of Notch2 and Notch3 on Cell Proliferation and Apoptosis of Trophoblast Cell Lines

Lycopene Alleviates Chronic Stress-Induced Spleen Apoptosis and Immunosuppression via Inhibiting the Notch Signaling Pathway in Rats

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