The Notch ligand, Delta-1, reduces TNF-α-induced growth suppression and apoptosis by decreasing activation of caspases in U937 cells

Murata-Ohsawa, Mai; Tohda, Shuji; Kogoshi, Hanae; Nara, Nobuo

doi:10.3892/ijmm.14.5.861

Cited by 6 publications

(6 citation statements)

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“…However, the mesectoderm is lost in early Dl RNAi embryos, and early neurogenic phenotypes are followed by caspase-mediated apoptosis of the ectopic neural tissue. Delta loss of function also enhances caspase-dependent apoptosis in flies and mice (Murata-Ohsawa et al, 2004;Müller et al, 2005). Loss of ventral tissue in Dl RNAi embryos is also apparent in previous studies on the function of Notch signalling in spider segmentation (Stollewerk et al, 2003;Schoppmeier and Damen, 2005).…”

Section: Research Articlementioning

confidence: 55%

Notch/Delta signalling is not required for segment generation in the basally branching insectGryllus bimaculatus

et al. 2011

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SUMMARYArthropods and vertebrates display a segmental body organisation along all or part of the anterior-posterior axis. Whether this reflects a shared, ancestral developmental genetic mechanism for segmentation is uncertain. In vertebrates, segments are formed sequentially by a segmentation 'clock' of oscillating gene expression involving Notch pathway components. Recent studies in spiders and basal insects have suggested that segmentation in these arthropods also involves Notch-based signalling. These observations have been interpreted as evidence for a shared, ancestral gene network for insect, arthropod and bilaterian segmentation. However, because this pathway can play multiple roles in development, elucidating the specific requirements for Notch signalling is important for understanding the ancestry of segmentation. Here we show that Delta, a ligand of the Notch pathway, is not required for segment formation in the cricket Gryllus bimaculatus, which retains ancestral characteristics of arthropod embryogenesis. Segment patterning genes are expressed before Delta in abdominal segments, and Delta expression does not oscillate in the pre-segmental region or in formed segments. Instead, Delta is required for neuroectoderm and mesectoderm formation; embryos missing these tissues are developmentally delayed and show defects in segment morphology but normal segment number. Thus, what initially appear to be 'segmentation phenotypes' can in fact be due to developmental delays and cell specification errors. Our data do not support an essential or ancestral role of Notch signalling in segment generation across the arthropods, and show that the pleiotropy of the Notch pathway can confound speculation on possible segmentation mechanisms in the last common bilaterian ancestor.

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Section: Research Articlementioning

confidence: 55%

Notch/Delta signalling is not required for segment generation in the basally branching insectGryllus bimaculatus

et al. 2011

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“…Yu and Song [47] found that Notch-1 signaling reduced cardiomyocyte apoptosis through regulating Bcl-2, Bax, and caspase-9/3. Murata et al [48] demonstrated that Notch activation induced by the recombinant delta-1 reduced the TNF-alpha-induced growth suppression and apoptosis in U937 cells.…”

Section: Discussionmentioning

confidence: 99%

JAG2/Notch2 inhibits intervertebral disc degeneration by modulating cell proliferation, apoptosis, and extracellular matrix

Long

Wang

et al. 2019

Arthritis Res Ther

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Background Intervertebral disc degeneration (IVDD)-related disorders are the major causes of low back pain. A previous study suggested that Notch activation serves as a protective mechanism and is a part of the compensatory response that maintains the necessary resident nucleus pulposus (NP) cell proliferation to replace lost or non-functional cells. However, the exact mechanism remains to be determined. In this study, we aimed to investigate the role of JAG2/Notch2 in NP cell proliferation and apoptosis. Methods Recombinant JAG2 or Notch2, Hes1, and Hey2 siRNAs were used to activate or inhibit Notch signaling. Cell proliferation, apoptosis, cell cycle regulatory factors, and pathways associated with Notch-mediated proliferation were examined. In vivo experiments involving an intradiscal injection of Sprague-Dawley rats were performed. Results Recombinant JAG2 induced Notch2 and Hes1/Hey2 expression together with NP cell proliferation. Downregulation of Notch2/Hes1/Hey2 induced G0/G1 phase cell cycle arrest in NP cells. Moreover, Notch2 mediated NP cell proliferation by regulating cyclin D1 and by activating PI3K/Akt and Wnt/β-catenin signaling. Furthermore, Notch signaling inhibited TNF-α-promoted NP cell apoptosis by suppressing the formation of the RIP1-FADD-caspase-8 complex. Finally, we found that intradiscal injection of JAG2 alleviated IVDD and that sh-Notch2 aggravated IVDD in a rat model. These results indicated that JAG2/Notch2 inhibited IVDD by modulating cell proliferation, apoptosis, and extracellular matrix. The JAG2/Notch2 axis regulated NP cell proliferation via PI3K/Akt and Wnt/β-catenin signaling and inhibited TNF-α-induced apoptosis by suppressing the formation of the RIP1-FADD-caspase-8 complex. Conclusions The current and previous results shed light on the therapeutic implications of targeting the JAG2/Notch2 axis to inhibit or reverse IVDD.

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“…TNF-stimulation activates MAP kinase cascades in some cell types, especially, the JNK signaling pathway [36][37][38]. There are crosstalks between JNK and NFκB in the TNF-α-induced signaling network.…”

Section: Discussionmentioning

confidence: 99%

TNF-α promotes cell survival through stimulation of K+ channel and NFκB activity in corneal epithelial cells

Wang

Reinach

2005

Experimental Cell Research

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Tumor necrosis factor (TNF-α) in various cell types induces either cell death or mitogenesis through different signaling pathways. In the present study, we determined in human corneal epithelial cells how TNF-α also promotes cell survival. Human corneal epithelial (HCE) cells were cultured in DMEM/F-12 medium containing 10% FBS. TNF-α stimulation induced activation of a voltage-gated K + channel detected by measuring single channel activity using patch clamp techniques. The effect of TNF-α on downstream events included NFκB nuclear translocation and increases in DNA binding activities, but did not elicit ERK, JNK, or p38 limb signaling activation. TNF-α induced increases in p21 expression resulting in partial cell cycle attenuation in the G 1 phase. Cell cycle progression was also mapped by flow cytometer analysis. Blockade of TNF-α-induced K + channel activity effectively prevented NFκB nuclear translocation and binding to DNA, diminishing the cell-survival protective effect of TNF-α. In conclusion, TNF-α promotes survival of HCE cells through sequential stimulation of K + channel and NFκB activities. This response to TNF-α is dependent on stimulating K + channel activity because following suppression of K + channel activity TNF-α failed to activate NFκB nuclear translocation and binding to nuclear DNA.

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The Notch ligand, Delta-1, reduces TNF-α-induced growth suppression and apoptosis by decreasing activation of caspases in U937 cells

Cited by 6 publications

References 0 publications

Notch/Delta signalling is not required for segment generation in the basally branching insectGryllus bimaculatus

Notch/Delta signalling is not required for segment generation in the basally branching insectGryllus bimaculatus

JAG2/Notch2 inhibits intervertebral disc degeneration by modulating cell proliferation, apoptosis, and extracellular matrix

TNF-α promotes cell survival through stimulation of K+ channel and NFκB activity in corneal epithelial cells

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