Enhancement of the endothelial production of prostacyclin by substituted derivatives of BAPTA-AM

Boeynaems, Jean‐Marie; Heilporn, Sylvie; Broeders, Fabienne; Braekman, Jean Claude

doi:10.1016/0014-2999(93)90343-g

Cited by 18 publications

(6 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…One potential caveat in the use of BAPTA analogues is whether they have the same off-target effects. There is evidence that they share the same off-target actions on the Na + /K + -ATPase [1], phospholipase C [31] and prostacyclin release [32]. An adjunct to the use of BAPTA to investigate the role of Ca 2+ signals in a cellular response could be pharmacological reagents that target specific Ca 2+ transport processes.…”

Section: Approach Utility Notesmentioning

confidence: 99%

Deleterious effects of calcium indicators within cells; an inconvenient truth

et al. 2018

View full text Add to dashboard Cite

The study of cellular Ca signalling is indebted to Roger Tsien for the invention of fluorescent indicators that can be readily loaded into living cells and provide the means to measure cellular Ca changes over long periods of time with sub-second resolution and microscopic precision. However, a recent study [1] reminds us that as useful as these tools are they need to be employed with caution as there can be off-target effects. This article summarises these recent findings within the wider context of confounding issues that can be encountered when using chemical and genetically-encoded Ca indicators, and briefly discusses some approaches that may mitigate against misleading outcomes.

show abstract

Section: Approach Utility Notesmentioning

confidence: 99%

Deleterious effects of calcium indicators within cells; an inconvenient truth

et al. 2018

View full text Add to dashboard Cite

show abstract

“…The intracellular Ca 2+ chelators have indeed complex side effects on Ca 2+ -dependent secretory mechanisms. In bovine aortic endothelial cells, BAPTA and Quin-2 could even increase the ATP-stimulated acid arachidonic release and PGI 2 production [12,36]. In rat thyroid cells, BAPTA has been demonstrated to prevent norepinephrine from increasing both [Ca 2+ ] i and arachidonic acid release [37].…”

Section: Discussionmentioning

confidence: 99%

Regulation of Arachidonic Acid Release by Calcium Influx in Human Endothelial Cells

et al. 1999

View full text Add to dashboard Cite

In response to stimuli, endothelial cells release arachidonic acid, a lipid precursor of various vasoactive substances. We have investigated the relationships between cytosolic Ca2+ movements and arachidonic acid release in human umbilical vein endothelial cells. Histamine, a receptor-dependent agonist, and thapsigargin, a specific inhibitor of sarco-/endoplasmic Ca2+ pumps, time- and dose-dependently increased the release of [1-14C]-arachidonic acid. This release was inhibited by AACOCF3, a selective inhibitor of cytosolic phospholipase A2 (PLA2). In the absence of Ca2+ influx, arachidonic acid release was suppressed in both histamine- and thapsigargin-stimulated cells, despite marked elevations of cytosolic Ca2+ concentration ([Ca2+]i). In the presence of Ca2+ influx, arachidonic acid release was reduced in cells treated with BAPTA, an intracellular Ca2+ buffer, or with SK&F 96365, a receptor-operated Ca2+ channel blocker. Arachidonic acid release was analyzed as a function of the two successive phases of Ca2+ response to stimulation: Ca2+ peak and plateau phase, reflecting Ca2+ mobilization from internal stores and Ca2+ influx, respectively. The amount of arachidonic acid released was directly related to [Ca2+]i values measured at the influx phase with a 80 nM [Ca2+]i threshold, similar to that reported for PLA2 translocation. This suggests that Ca2+ entry from the extracellular space is essential for activating cytosolic PLA2 in human endothelial cells.

show abstract

“…To elucidate whether Ca 2+ is required for COX-2 expression and PGE 2 synthesis, HTSMCs were preincubated with 30 ÌM BAPTA-AM (a potent intracellular Ca 2+ chelator) [6] and 1 mM EDTA, and then stimulated with IL-1ß. Results in figure 6 demonstrate that pretreatment of these cells with BAPTA-AM and EDTA reduced COX-2 expression and PGE 2 synthesis when they were exposed to IL-1ß (p !…”

Section: Effect Of Ca 2+ On Il-1ß-induced Cox-2 Expression and Pge 2 mentioning

confidence: 99%

Induction of Cyclooxygenase-2 Expression in Human Tracheal Smooth Muscle Cells by Interleukin-1β: Involvement of p42/p44 and p38 Mitogen-Activated Protein Kinases and Nuclear Factor-κB

Lin¹,

Sun²,

Luo³

et al. 2004

J Biomed Sci

View full text Add to dashboard Cite

Interleukin-1β (IL-1β) has been recognized as a potent stimulus for the synthesis of prostaglandin (PG), which has been implicated in inflammatory responses of the airways. However, the mechanisms underlying IL-1β-induced cyclooxygenase (COX) expression and PGE₂ synthesis via activation of p42/p44 and p38 mitogen-activated protein kinases (MAPKs) in human tracheal smooth muscle cells (HTSMCs) are not completely understood. We found that IL-1β increased COX-2 expression and PGE₂ synthesis in time- and concentration-dependent manners. Both specific phosphatidylcholine-phospholipase C inhibitor (D609) and protein kinase C inhibitor (GF109203X) attenuated IL-1β-induced responses in HTSMCs. IL-1β-induced COX-2 expression and PGE₂ synthesis were also inhibited by an inhibitor of MEK1/2 (PD98059) and inhibitors of p38 MAPK (SB203580 and SB202190), respectively, suggesting the involvement of p42/p44 and p38 MAPKs in these responses. This hypothesis was further supported by the transient activation of p42/p44 and p38 MAPKs induced by IL-1β. Furthermore, IL-1β-induced activation of nuclear factor-ĸB (NF-ĸB) was inversely correlated with the degradation of IĸB-α in HTSMCs. IL-1β-induced COX-2 expression and PGE₂ synthesis were inhibited by the NF-ĸB inhibitor pyrrolidinedithiocarbamate. These findings suggest that the expression of COX-2 is correlated with the release of PGE₂ from IL-1β-challenged HTSMCs, which is mediated, at least in part, through p42/p44 and p38 MAPKs and NF-ĸB signaling pathways in HTSMCs.

show abstract

Enhancement of the endothelial production of prostacyclin by substituted derivatives of BAPTA-AM

Cited by 18 publications

References 19 publications

Deleterious effects of calcium indicators within cells; an inconvenient truth

Deleterious effects of calcium indicators within cells; an inconvenient truth

Regulation of Arachidonic Acid Release by Calcium Influx in Human Endothelial Cells

Induction of Cyclooxygenase-2 Expression in Human Tracheal Smooth Muscle Cells by Interleukin-1β: Involvement of p42/p44 and p38 Mitogen-Activated Protein Kinases and Nuclear Factor-κB

Contact Info

Product

Resources

About

Enhancement of the endothelial production of prostacyclin by substituted derivatives of BAPTA-AM

Cited by 18 publications

References 19 publications

Deleterious effects of calcium indicators within cells; an inconvenient truth

Deleterious effects of calcium indicators within cells; an inconvenient truth

Regulation of Arachidonic Acid Release by Calcium Influx in Human Endothelial Cells

Induction of Cyclooxygenase-2 Expression in Human Tracheal Smooth Muscle Cells by Interleukin-1&beta;: Involvement of p42/p44 and p38 Mitogen-Activated Protein Kinases and Nuclear Factor-&kappa;B

Contact Info

Product

Resources

About

Induction of Cyclooxygenase-2 Expression in Human Tracheal Smooth Muscle Cells by Interleukin-1β: Involvement of p42/p44 and p38 Mitogen-Activated Protein Kinases and Nuclear Factor-κB