Caspases regulate VAMP-8 expression and phagocytosis in dendritic cells

Ho, Yong; Cai, Deyu Tarika; Huang, Dachuan; Wang, Cheng Chun; Wong, Siew Heng

doi:10.1016/j.bbrc.2009.07.028

Cited by 18 publications

(24 citation statements)

References 26 publications

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“…These results suggest that the pyrogallol-type structure, such as the pyrogalloltype B-ring or galloyl group, is an important factor in the phagocytic activity of VD3-differentiated HL60 cells. This is similar to the results of Yamada et al (1997), who showed that pyrogallol-type polyphenols, such as EGCG, gallic acid and pyrogallol, enhanced Polyphenols with a pyrogallol-type structure induce the apoptosis of malignant cells through a caspase signaling pathway (Saeki et al 2000;Hayakawa et al 2001;Vergote et al 2002); however, caspase is a protease playing an important role not only in apoptosis but also in innate immunity (Martinon and Tschopp 2004;Winoto 2004), and regulates phagocytic activity in macrophages, such as dendritic cells (Ho et al 2009); therefore, we investigated the involvement of the caspase pathway in phagocytic activity. As shown in Fig.…”

Section: Resultssupporting

confidence: 83%

“…Lipopolysaccharide (LPS), b-glucan, peptidoglycan, lipopeptide, and nucleic acid are well known ligands binding to these innate immune receptors (Peiser and Gordon 2001;Underhill and Gantner 2004;Rock et al 1998;Dunne and O'Neill 2003). Recently, it was reported that caspase signaling also regulates phagocytic activity in macrophages, such as dendritic cells (Ho et al 2009). It is known that green tea polyphenols induce caspase activation (Saeki et al 2000;Hayakawa et al 2001;Vergote et al 2002;Hsu et al 2007), but phagocytosis induction by green tea polyphenols through caspase signaling has not been investigated.…”

Section: Introductionmentioning

confidence: 98%

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Enhancement of phagocytic activity of macrophage-like cells by pyrogallol-type green tea polyphenols through caspase signaling pathways

Monobe¹,

Ema²,

Tokuda³

et al. 2010

Cytotechnology

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We investigated the phagocytosis-enhancing activity of green tea polyphenols, such as epigallocatechin gallate (EGCG), epigallocatechin (EGC), epicatechin gallate (ECG), epicatechin (EC) catechin (+C) and strictinin, using VD3-differentiated HL60 cells. EGCG, EGC, ECG and strictinin, but not EC and +C, increased the phagocytic activity of macrophage-like cells, and a caspase inhibitor significantly inhibited phagocytic activities. These results suggest that the pyrogallol-type structure in green tea polyphenols may be important for enhancement of the phagocytic activity through caspase signaling pathways.

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Section: Resultssupporting

confidence: 83%

Section: Introductionmentioning

confidence: 98%

Enhancement of phagocytic activity of macrophage-like cells by pyrogallol-type green tea polyphenols through caspase signaling pathways

Monobe¹,

Ema²,

Tokuda³

et al. 2010

Cytotechnology

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“…# P < 0.06; *P < 0.05; **P < 0.01; ***P < 0.001. synaptogenesis, synaptic contact, and transmission of nerve impulses (SI Appendix, Table S7). Using qRT-PCR, we confirmed the differences in expression of glutamate transporter, solute carrier family 1, member 1 (Slc1a1) (∼1.9-fold increase) (20,(57)(58)(59), acetylcholinesterase (AChE) (∼1.4-fold increase) (60,61), cholinergic receptor nicotinic beta polypeptide 1 (Chrnb1) (2.0-fold increase) (62), Cortactin (Cttn) (∼1.4-fold increase) (63)(64)(65)(66)(67) (72)(73)(74), vesicle-associated membrane protein 8 (VAMP8) (∼1.8-fold increase) (75)(76)(77)(78)(79)(80), presenilin 2 (Psen2) (81-86) (∼1.5-fold increase), and calcium channel, voltage-dependent, alpha 2/delta subunit 3 (Cacna2d3) (∼1.7-fold decrease) (39, 87-90) (SI Appendix, Tables S7, S10, and S11). Slc1a1, Cttn, Chrnb1, and Psen2 are experimentally confirmed and/or predicted targets for members of miR-183/96/182 (20, 91) (SI Appendix, Table S7B), suggesting that miR-183/96/182 directly regulates the expression of these genes.…”

Section: Discussionmentioning

confidence: 99%

Inactivation of the microRNA-183/96/182cluster results in syndromic retinal degeneration

Lumayag

Haldin

Corbett

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

175

241

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The microRNA-183/96/182 cluster is highly expressed in the retina and other sensory organs. To uncover its in vivo functions in the retina, we generated a knockout mouse model, designated "miR-183CGT/GT ," using a gene-trap embryonic stem cell clone. We provide evidence that inactivation of the cluster results in early-onset and progressive synaptic defects of the photoreceptors, leading to abnormalities of scotopic and photopic electroretinograms with decreased b-wave amplitude as the primary defect and progressive retinal degeneration. In addition, inactivation of the miR-183/96/ 182 cluster resulted in global changes in retinal gene expression, with enrichment of genes important for synaptogenesis, synaptic transmission, photoreceptor morphogenesis, and phototransduction, suggesting that the miR-183/96/182 cluster plays important roles in postnatal functional differentiation and synaptic connectivity of photoreceptors. M icroRNAs (miRNAs) are small, endogenous, noncoding, regulatory RNAs and represent a newly recognized level of gene-expression regulation (1-4). miRNAs have unique expression profiles in the developing and adult retina and are involved in normal development and functions of the retina in all species studied so far (5-12). miRNAs are dysregulated in the retina of retinal degenerative mouse models, suggesting their potential involvement in retinal degeneration (13,14). Conditional inactivation of dicer, an RNase III endonuclease required for miRNA maturation in cytosol (15), in the mouse retina resulted in alteration of retinal differentiation and optic-cup patterning, increased cell death, and disorganization of axons of retinal ganglion cells (16)(17)(18)(19), suggesting that miRNAs are important for normal development and functions of the mammalian retina. However, in vivo functions of individual miRNAs in the retina still are largely unknown.Previously, we identified a highly conserved, intergenic, sensory organ-specific, paralogous miRNA cluster, the miR-183/96/182 cluster (hereafter, miR-183/96/182), contained within an ∼4-kb genomic segment on mouse chr6qA3.3 (8, 9). In the adult retina, miR-183/96/182 is expressed specifically in all photoreceptors and in the inner nuclear layer (8, 10). Developmentally, its expression is minimal in the embryonic retina but increases dramatically after birth and peaks in the adult retina, suggesting a role for miR-183/ 96/182 in maturation and normal functioning of the adult retina (8, 9). Additionally, expression of miR-183/96/182 has a diurnal pattern, suggesting a potential role in rhythmic functions of the retina (8, 9). Recently, miR-183/96/182 also was shown to be light responsive, independent of the circadian cycle (20). Targeted deletion of miR-182 alone in mouse did not result in a discernible phenotype, suggesting functional compensation by miR-183 and miR-96 (21). Point mutations of miR-96 were reported to result in progressive, nonsyndromic hearing loss in both human (22) and mouse (23); however, there was no apparent retinal phenotype, an ob...

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“…Recent studies have revealed unanticipated connections between the SNARE machinery and apoptosis. For example, expression of several SNARE components was found to be regulated by key apoptotic molecules, such as p53 (22) and caspases (23). On the other hand, SNARE proteins themselves can either suppress or accelerate apoptosis (22,24,25).…”

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confidence: 99%

Loss of Soluble N-Ethylmaleimide-sensitive Factor Attachment Protein α (αSNAP) Induces Epithelial Cell Apoptosis via Down-regulation of Bcl-2 Expression and Disruption of the Golgi

Naydenov

Harris

Brown

et al. 2012

Journal of Biological Chemistry

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Background: Vesicle trafficking proteins play important roles in regulating cell survival. Results: Inhibition of a key membrane fusion protein, ␣SNAP, induced epithelial cell apoptosis, decreased Bcl-2 level, and impaired ER-Golgi communications. Conclusion: ␣SNAP promotes cell survival by controlling ER/Golgi-dependent expression of Bcl-2. Significance: Uncovering mechanisms that link vesicle trafficking and apoptosis is critical for understanding the regulation of cell fate.

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Caspases regulate VAMP-8 expression and phagocytosis in dendritic cells

Cited by 18 publications

References 26 publications

Enhancement of phagocytic activity of macrophage-like cells by pyrogallol-type green tea polyphenols through caspase signaling pathways

Enhancement of phagocytic activity of macrophage-like cells by pyrogallol-type green tea polyphenols through caspase signaling pathways

Inactivation of the microRNA-183/96/182cluster results in syndromic retinal degeneration

Loss of Soluble N-Ethylmaleimide-sensitive Factor Attachment Protein α (αSNAP) Induces Epithelial Cell Apoptosis via Down-regulation of Bcl-2 Expression and Disruption of the Golgi

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