Growth factor-like action of lysophosphatidic  acid on human B lymphoblasts

Rosskopf, Dieter; Daelman, Wim; Busch, Stefan; Schürks, Markus; Hartung, Kathrin; Kribben, Andreas; Michel, Martin C.; Siffert, Winfried

doi:10.1152/ajpcell.1998.274.6.c1573

Cited by 43 publications

(26 citation statements)

References 44 publications

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“…The assay of LPA-stimulated Ca 2 þ mobilization was performed as previously described (Rosskopf et al, 1998) with modifications. Briefly, cells (1-3 Â 10 6 /ml in RPMI-1640) were loaded with Fura-2-AM (1 mM) or treated with an equivalent volume of DMSO (1 ml/ ml cell suspension; blank sample) as previously described (Emamghoreishi et al, 1997).…”

Section: Ca 2 þ Mobilization Assaysmentioning

confidence: 99%

Chronic Lithium Treatment Attenuates Intracellular Calcium Mobilization

Wasserman

Corson

Sibony

et al. 2004

Neuropsychopharmacol

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Elevated basal intracellular calcium (Ca 2 þ ) levels ([Ca 2 þ ] B ) in B lymphoblast cell lines (BLCLs) from bipolar I disorder (BD-I) patients implicate altered Ca 2 þ homeostasis in this illness. Chronic lithium treatment affects key proteins modulating intracellular Ca 2 þ signaling. Thus, we sought to determine if chronic exposure to therapeutic lithium concentrations also modifies intracellular Ca 2 þ homeostasis in this surrogate cellular model of signal transduction disturbances in BD. BLCLs from BD-I (N ¼ 26) and healthy subjects (N ¼ 17) were regrown from frozen stock and incubated with 0.75 mM lithium or vehicle for 24 h (acute) or 7 days (chronic). [Ca 2 þ ] B , lysophosphatidic acid (LPA)-stimulated Ca 2 þ mobilization ([Ca 2 þ ] S ), and thapsigargin-induced store-operated Ca 2 þ entry (SOCE) were determined using ratiometric fluorometry with Fura-2. Compared with vehicle, chronic lithium exposure resulted in significantly higher [Ca 2 þ ] B (F ¼ 8.47; p ¼ 0.006) in BLCLs from BD-I and healthy subjects. However, peak LPA-stimulated [Ca 2 þ ] S and SOCE were significantly reduced (F ¼ 11.1, p ¼ 0.002 and F ¼ 8.36, p ¼ 0.007, respectively). Acute lithium exposure did not significantly affect measured parameters. In summary, the effect of chronic lithium to elevate [Ca 2 þ ] B in BLCLs while attenuating both receptor-stimulated and SOCE components of intracellular Ca 2 þ mobilization in BLCLs suggests that modulation of intracellular Ca 2 þ homeostasis may be important to the therapeutic action of lithium.

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Section: Ca 2 þ Mobilization Assaysmentioning

confidence: 99%

Chronic Lithium Treatment Attenuates Intracellular Calcium Mobilization

Wasserman

Corson

Sibony

et al. 2004

Neuropsychopharmacol

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“…For instance, LPA has chemotactic activity, regulates secretion of IL-2, and prevents apoptosis in T cells (16 -18). In addition, LPA is a growth factor for B cells, and it stimulates adhesion of monocytes and neutrophils to endothelial cells (19,20).…”

Section: Ysophosphatidic Acid (Lpa)mentioning

confidence: 99%

The Influence of Lysophosphatidic Acid on the Functions of Human Dendritic Cells

Panther

Idzko

Corinti

et al. 2002

The Journal of Immunology

103

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Lysophosphatidic acid (LPA) is a bioactive lipid mediator which is generated by secretory phospholipase A2. In this study, we studied the biological activity of LPA on human dendritic cells (DCs), which are specialized APCs characterized by their ability to migrate into target sites and secondary lymphoid organs to process Ags and activate naive T cells. We show that immature and mature DCs express the mRNA for different LPA receptors such as endothelial differentiation gene (EDG)-2, EDG-4, and EDG-7. In immature DCs, LPA stimulated pertussis toxin-sensitive Ca2+ increase, actin polymerization, and chemotaxis. During the maturation process, DCs lost their ability to respond toward LPA with Ca2+ transients, actin polymerization, and chemotaxis. However, LPA inhibited in a pertussis toxin-insensitive manner the secretion of IL-12 and TNFα as well as enhanced secretion of IL-10 from mature DCs. Moreover, LPA did not affect the endocytic or phagocytic capacities and the surface phenotype of DCs, although it increased the allostimulatory function of mature DC and inhibited their capacity to induce Th1 differentiation. In summary, our study implicates that LPA might regulate the trafficking, cytokine production, and T cell-activating functions of DCs.

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“…In addition, we also conducted studies with cells that had been serum starved for 24 h before infection. In several studies investigating the effects of specific agonists on mammalian cell signaling, cells were cultured in the absence of serum before signaling studies were conducted (37). Withdrawal of serum serves two purposes, (i) to synchronize cells into the G 0 phase and (ii) to distinguish between specific agonist-induced signaling and that mediated by lysophosphatidic acid (LPA).…”

Section: Serovar Typhimurium Induces Jnk and Erk Activation Inmentioning

confidence: 99%

Proteolytic Inhibition ofSalmonella entericaSerovar Typhimurium-Induced Activation of the Mitogen-Activated Protein Kinases ERK and JNK in Cultured Human Intestinal Cells

2002

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Bromelain, a mixture of cysteine proteases from pineapple stems, blocks signaling by the mitogen-activated protein (MAP) kinases extracellular regulated kinase 1 (ERK-1) and ERK-2, inhibits inflammation, and protects against enterotoxigenic Escherichia coli infection. In this study, we examined the effect of bromelain on Salmonella enterica serovar Typhimurium infection, since an important feature of its pathogenesis is its ability to induce activation of ERK-1 and ERK-2, which leads to internalization of bacteria and induction of inflammatory responses. Our results show that bromelain dose dependently blocks serovar Typhimuriuminduced ERK-1, ERK-2, and c-Jun NH 2 -terminal kinase (JNK) activation in Caco-2 cells. Bromelain also blocked signaling induced by carbachol and anisomycin, pharmacological MAP kinase agonists. Despite bromelain inhibition of serovar Typhimurium-induced MAP kinase signaling, it did not prevent subsequent invasion of the Caco-2 cells by serovar Typhimurium or alter serovar Typhimurium -induced decreases in resistance across Caco-2 monolayers. Surprisingly, bromelain also did not block serovar Typhimuriuminduced interleukin-8 (IL-8) secretion but synergized with serovar Typhimurium to enhance IL-8 production. We also found that serovar Typhimurium does not induce ERK phosphorylation in Caco-2 cells in the absence of serum but that serovar Typhimurium-induced invasion and decreases in monolayer resistance are unaffected. Collectively, these data indicate that serovar Typhimurium-induced invasion of Caco-2 cells, changes in the resistance of epithelial cell monolayers, and IL-8 production can occur independently of the ERK and JNK signaling pathways. Data also confirm that bromelain is a novel inhibitor of MAP kinase signaling pathways and suggest a novel role for proteases as inhibitors of signal transduction pathways in intestinal epithelial cells.

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Growth factor-like action of lysophosphatidic acid on human B lymphoblasts

Cited by 43 publications

References 44 publications

Chronic Lithium Treatment Attenuates Intracellular Calcium Mobilization

Chronic Lithium Treatment Attenuates Intracellular Calcium Mobilization

The Influence of Lysophosphatidic Acid on the Functions of Human Dendritic Cells

Proteolytic Inhibition ofSalmonella entericaSerovar Typhimurium-Induced Activation of the Mitogen-Activated Protein Kinases ERK and JNK in Cultured Human Intestinal Cells

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