Modulation of neutrophil apoptosis by β-amyloid proteins

Park, Hae Young; Park, Joo-In; Baek, Dae-Won; Lee, Sun-Young; Lee, Min-Jung; Kim, Ja-Woong; Hong, Young-Seoub; Lee, Yong-Hwan; Kwak, Jong‐Young

doi:10.1016/j.intimp.2006.01.019

Cited by 10 publications

(7 citation statements)

References 36 publications

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“…Amyloid precursor peptides including the toxic Aß 1-42 fragment have previously been shown to induce apoptosis in a variety of cells such as neurons [1][2][3][4][5][6], pancreatic islet cells [7,8], endothelial cells [9] and neutrophils [10]. Mechanisms implicated in amyloid 176 induced apoptosis include Ca 2+ entry [10], calpain activation [5], oxidative stress [1,2,4] and ceramide formation [3].…”

Section: Introductionmentioning

confidence: 99%

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Amyloid Induced Suicidal Erythrocyte Death

Nicolay

Gatz

Liebig

et al. 2007

Cell Physiol Biochem

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Amyloid peptides are known to induce apoptosis in a wide variety of cells. Erythrocytes may similarly undergo suicidal death or eryptosis, which is characterized by scrambling of the cell membrane with subsequent exposure of phosphatidylserine (PS) at the cell surface. Eryptosis is triggered by increase of cytosolic Ca²⁺ activity and by activation of acid sphingomyelinase with subsequent formation of ceramide. Triggers of eryptosis include energy depletion and isosmotic cell shrinkage (replacement of extracellular Cl^- by impermeable gluconate for 24 h). The present study explored whether amyloid peptide Aβ _1-42 could trigger eryptosis and to possibly identify underlying mechanisms. Erythrocytes from healthy volunteers were exposed to amyloid and PS-exposure (annexin V binding), cell volume (forward scatter), cytosolic Ca²⁺ activity (Fluo3 fluorescence) and ceramide formation (anti-ceramide antibody) were determined by FACS analysis. Exposure of erythrocytes to the amyloid peptide Aβ _1-42 (? 0.5 µM) for 24 h significantly triggered annexin V binding, an effect mimicked to a lesser extent by the amyloid peptide Aβ _1-40 (1 µM). Aβ _1-42 (? 1.0 µM) further significantly decreased forward scatter of erythrocytes. The effect of Aβ _1-42 (? 0.5 µM) on erythrocyte annexin V binding was paralleled by formation of ceramide but not by significant increase of cytosolic Ca²⁺ activity. The presence of Aβ _1-42 further significantly enhanced the eryptosis following Cl^- depletion but not of glucose depletion for 24 hours. The present observations disclose a novel action of Aβ _1-42, which may well contribute to the pathophysiological effects of amyloid peptides, such as vascular complications in Alzheimer''s disease.

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Section: Introductionmentioning

confidence: 99%

“…Mechanisms implicated in amyloid 176 induced apoptosis include Ca 2+ entry [10], calpain activation [5], oxidative stress [1,2,4] and ceramide formation [3].…”

Section: Introductionmentioning

confidence: 99%

Amyloid Induced Suicidal Erythrocyte Death

Nicolay

Gatz

Liebig

et al. 2007

Cell Physiol Biochem

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“…Genes with a positive effect on apoptosis include CASP8, an initiator caspase involved in death receptor-mediated apoptosis stimulated by FasL, TNF␣ or tumour necrosis factor-related apoptosis-inducing ligand (Mocarski et al, 2011;Monie and Bryant, 2015); TG2, a multifunctional gene that has been implicated in apoptotic cell clearance (Nadella et al, 2015); and RARA, which has been associated with neutrophil differentiation and apoptosis (Kastner and Chan, 2001). Among the genes related to anti-apoptotic activity, we observed upregulation of those coding for DHCR24, a gene that when is overexpressed can protect the cells from apoptosis induced by oxidative stress (Lu et al, 2008), A4, which delays the apoptotic rate of human neutrophils (Park et al, 2006), and ADORA2A, which induces a delay in spontaneous apoptosis of human neutrophils (Pliyev et al, 2014). Vaccines containing the same adjuvants as tested in the present study induced generation of numerous apoptotic neutrophils in the peritoneal cavity of turbot (Noia et al, 2014).…”

Section: Regulation Of Apoptosismentioning

confidence: 84%

Vaccine-induced modulation of gene expression in turbot peritoneal cells. A microarray approach

Fontenla

Blanco-Abad

Pardo

et al. 2016

Molecular Immunology

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We used a microarray approach to examine changes in gene expression in turbot peritoneal cells after injection of the fish with vaccines containing the ciliate parasite Philasterides dicentrarchi as antigen and one of the following adjuvants: chitosan-PVMMA microspheres, Freund́s complete adjuvant, aluminium hydroxide gel or Matrix-Q (Isconova, Sweden). We identified 374 genes that were differentially expressed in all groups of fish. Forty-two genes related to tight junctions and focal adhesions and/or actin cytoskeleton were differentially expressed in free peritoneal cells. The profound changes in gene expression related to cell adherence and cytoskeleton may be associated with cell migration and also with the formation of cell-vaccine masses and their attachment to the peritoneal wall. Thirty-five genes related to apoptosis were differentially expressed. Although most of the proteins coded by these genes have a proapoptotic effect, others are antiapoptotic, indicating that both types of signals occur in peritoneal leukocytes of vaccinated fish. Interestingly, many of the genes related to lymphocytes and lymphocyte activity were downregulated in the groups injected with vaccine. We also observed decreased expression of genes related to antigen presentation, suggesting that macrophages (which were abundant in the peritoneal cavity after vaccination) did not express these during the early inflammatory response in the peritoneal cavity. Finally, several genes that participate in the inflammatory response were differentially expressed, and most participated in resolution of inflammation, indicating that an M2 macrophage response is generated in the peritoneal cavity of fish one day post vaccination.

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“…Amyloid peptides may be effective through stimulation of Ca 2? entry [10,38,39], calpain [7], oxidative stress [3,4,6], p38 kinase activation [40], MAP kinase activation [27], c-Jun [41], p53 and p21WAF1/CIP1 [42] and, as shown in other cells, by ceramide formation [5].…”

Section: Introductionmentioning

confidence: 80%

“…Amylin is a hormone cosecreted in pancreatic ß cells after a meal and has a complementary action to insulin [2]. Amyloid precursor peptides, such as Aß 1-42 fragment, trigger suicidal death in a variety of cells including neurons [3][4][5][6][7][8], endothelial cells [9], neutrophils [10], erythrocytes [11] and pancreatic beta cells [12,13]. Compelling evidence suggests that membrane permeable oligomers of amylin may be cytotoxic and responsible for the reduction of beta cell mass during the development of type 2 diabetes mellitus [14][15][16].…”

Section: Introductionmentioning

confidence: 99%

Sphingomyelinase dependent apoptosis following treatment of pancreatic beta-cells with amyloid peptides Aß1-42 or IAPP

et al. 2009

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Amyloid peptides interfere with survival of pancreatic beta-cells. In some cells apoptosis is paralleled by ceramide-dependent alterations of ion channel activity. The purpose of the present study was to elucidate the dependence of amyloid peptides Abeta(1-42) and islet amyloid polypeptide (IAPP)-induced cell death on ceramide formation and ion channel activity in murine pancreatic islet cells. As disclosed by TUNEL (terminal dUTP nick-end labelling) and cleaved caspase 3 staining, apoptotic cell death was induced by Abeta(1-42), IAPP and exogenously added C2-ceramide in islet cells from wild type mice. In islet cells from acid sphingomyelinase-deficient mice (ASMKO) Abeta(1-42) and IAPP but not exogenously added N-acetyl-D-sphingosine (C2-ceramide, 20 microM) failed to stimulate apoptosis. Immunofluorescent staining revealed a stimulatory effect of Abeta(1-42) on ceramide formation. According to patch clamp experiments, administration of Abeta(1-42) and IAPP significantly decreased outwardly rectifying whole cell currents in wild type but not in ASMKO islet cells. C2-ceramide but not inactive di-ceramide (20 microM) mimicked the inhibitory effect on Kv channel current. In conclusion, amyloid peptides induce apoptosis of pancreatic islet cells at least in part through activation of acid sphingomyelinase resulting in production of ceramide and subsequent inhibition of ion channel activity.

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Modulation of neutrophil apoptosis by β-amyloid proteins

Cited by 10 publications

References 36 publications

Amyloid Induced Suicidal Erythrocyte Death

Amyloid Induced Suicidal Erythrocyte Death

Vaccine-induced modulation of gene expression in turbot peritoneal cells. A microarray approach

Sphingomyelinase dependent apoptosis following treatment of pancreatic beta-cells with amyloid peptides Aß1-42 or IAPP

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