A plethora of interacting organellar Ca2+ stores

Michelangeli, Francesco; Ogunbayo, Oluseye A.; Wootton, Laura L.

doi:10.1016/j.ceb.2005.01.005

Cited by 84 publications

(75 citation statements)

References 44 publications

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“…Although we have yet to identify the source, this finding is similar to one we previously described in human PAEC treated with histamine where pretreatment with caffeine, ryanodine, bafilomycin, and FCCP did not abolish histamine-induced Ca 2ϩ transients in PAEC (23). While the ER/SR represent the largest intracellular store in most excitable and nonexcitable cells (including PASMC and PAEC), mitochondria, Golgi apparatus, lysosomes, peroxisomes, and endosomes all represent other potential Ca 2ϩ sources (25). We did observe equivalent results in response to thrombin using a similar cocktail (i.e., caffeine, ryanodine, bafilomycin, and FCCP) (Agange and Yuan, unpublished observations).…”

Section: Discussionsupporting

confidence: 56%

Thrombin-mediated increases in cytosolic [Ca²⁺] involve different mechanisms in human pulmonary artery smooth muscle and endothelial cells

Sacks¹,

Firth²,

Remillard³

et al. 2008

American Journal of Physiology-Lung Cellular and Molecular Phys

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Sacks RS, Firth AL, Remillard CV, Agange N, Yau J, Ko EA, Yuan JX. Thrombin-mediated increases in cytosolic [Ca 2ϩ ] involve different mechanisms in human pulmonary artery smooth muscle and endothelial cells. Am J Physiol Lung Cell Mol Physiol 295: L1048 -L1055, 2008. First published October 3, 2008 doi:10.1152/ajplung.90259.2008.-Thrombin is a procoagulant inflammatory agonist that can disrupt the endothelium-lumen barrier in the lung by causing contraction of endothelial cells and promote pulmonary cell proliferation. Both contraction and proliferation require increases in cytosolic Ca 2ϩ concentration ([Ca 2ϩ ]cyt). In this study, we compared the effect of thrombin on Ca 2ϩ signaling in human pulmonary artery smooth muscle (PASMC) and endothelial (PAEC) cells. Thrombin increased the [Ca 2ϩ ]cyt in both cell types; however, the transient response was significantly higher and recovered quicker in the PASMC, suggesting different mechanisms may contribute to thrombin-mediated increases in [Ca 2ϩ ]cyt in these cell types. Depletion of intracellular stores with cyclopiazonic acid (CPA) in the absence of extracellular Ca 2ϩ induced calcium transients representative of those observed in response to thrombin in both cell types. Interestingly, CPA pretreatment significantly attenuated thrombin-induced Ca 2ϩ release in PASMC; this attenuation was not apparent in PAEC, indicating that a PAEC-specific mechanism was targeted by thrombin. Treatment with a combination of CPA, caffeine, and ryanodine also failed to abolish the thrombin-induced Ca 2ϩ transient in PAEC. Notably, thrombin-induced receptor-mediated calcium influx was still observed in PASMC after CPA pretreatment in the presence of extracellular Ca 2ϩ . Ca 2ϩ oscillations were triggered by thrombin in PASMC resulting from a balance of extracellular Ca 2ϩ influx and Ca 2ϩ reuptake by the sarcoplasmic reticulum. The data show that thrombin induces increases in intracellular calcium in PASMC and PAEC with a distinct CPA-, caffeine-, and ryanodineinsensitive release existing only in PAEC. Furthermore, a dynamic balance between Ca 2ϩ influx, intracellular Ca 2ϩ release, and reuptake underlie the Ca 2ϩ transients evoked by thrombin in some PASMC. Understanding of such mechanisms will provide an important insight into thrombin-mediated vascular injury during hypertension. sarcoplasmic and endoplasmic reticulum; Ca 2ϩ store THROMBIN, A MAJOR EFFECTOR PROTEASE of the coagulation cascade, is best known for its role in the conversion of fibrinogen into fibrin. Thrombin can operate as an inflammatory agent by stimulating endothelial cells (EC) to produce and/or secrete chemotactic factors by promoting monocyte recruitment and by increasing endothelial permeability (8, 9). At the same time, thrombin regulates the inflammation processes by blocking aggregation of platelets, adhesion of monocytes to endothelium, and by releasing nitric oxide (NO) from EC (35). In the lung, thrombin has a number of effects not limited to coagulation, which may play significant roles in ...

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Section: Discussionsupporting

confidence: 56%

Thrombin-mediated increases in cytosolic [Ca²⁺] involve different mechanisms in human pulmonary artery smooth muscle and endothelial cells

Sacks¹,

Firth²,

Remillard³

et al. 2008

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…The regulation of intracellular Ca 2ϩ stores in insulinsecreting cells is complex (29). There are several Ca 2ϩ storage pools that can be discharged independently or semi-independently via various agonists.…”

Section: Discussionmentioning

confidence: 99%

Inositol (1,4,5)-Trisphosphate Dynamics and Intracellular Calcium Oscillations in Pancreatic β-Cells

et al. 2005

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Glucose-stimulated insulin secretion is associated with transients of intracellular calcium concentration ([Ca2؉is an important signaling mechanism in the glucose-stimulated ␤-cell (10,11). ␤-Cells have been shown to contain inositol 1,4,5-trisphosphate [Ins(1,4,5)P 3 ] receptors (12), ryanodine receptors (4,10), and Ca 2ϩ channels gated by cyclic ADP-ribose (13) or nicotinic acid adenine dinucleotide phosphate (14,15). Ins(1,4,5)P 3 -dependent mobilization of endoplasmic reticulum Ca 2ϩ has been well described in ␤-cells as part of the response to various agonists, such as acetylcholine, purine nucleotides, or histamines. However, it is still unclear whether Ins(1,4,5)P 3 signaling is important in glucose-dependent ␤-cell activation, particularly for [Ca 2ϩ ] i oscillations. Our simulations of ␤-cell calcium responses, taking into account ATP and Na ϩ homeostasis as well as uptake and release of Ca 2ϩ by the endoplasmic reticulum, indicate that Ca 2ϩ in the endoplasmic reticulum is one of the main variables driving [Ca 2ϩ ] i oscillations (16). Our model suggested that the effect of regulated Ca 2ϩ efflux from the intracellular stores could shape the pattern of slow calcium oscillations. Using a biosensor capable of reporting Ins(1,4,5)P 3 (17) and confocal microscopy, we have demonstrated dynamics of Ins(1,4,5)P 3 in mouse primary ␤-cells and in MIN6 insulinoma cells upon stimulation with glucose and carbamoylcholine (CCh), as well as depolarization with KCl. We show that Ins(1,4,5)P 3 concentration oscillates in parallel with [Ca 2ϩ ] i in response to glucose stimulation, but it is not the driving force for [Ca 2ϩ ] i oscillations. RESEARCH DESIGN AND METHODSIsolation and culturing of mouse islets of Langerhans and islet cells. Islets were isolated from the pancreata of 1-to 5-month-old C57BL/J6 mice (The Jackson Laboratories) as described previously (7

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“…Ca 2+ -transients govern a variety of cellular phenomena, some occurring on a sub-second time scale [1][2][3], by different mechanisms for Ca 2+ mobilisation and subsequent re-establishment of Ca 2+ homeostasis [4][5][6]. In ciliated protozoans, specifically in Paramecium, Ca 2+ regulates dense-core secretory vesicle (trichocyst) exocytosis [7,8] and ciliary beat [9][10][11], notably depolarisation-induced ciliary beat reversal [12,13], among other phenomena [14].…”

Section: Introductionmentioning

confidence: 99%

Sub-second calcium coupling between outside medium and subplasmalemmal stores during overstimulation/depolarisation-induced ciliary beat reversal in Paramecium cells

et al. 2006

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As amply documented by electrophysiology, depolarisation in Paramecium induces a Ca 2+ influx selectively via ciliary voltage-dependent Ca 2+ -channels, thus inducing ciliary beat reversal. Subsequent downregulation of ciliary Ca 2+ has remained enigmatic. We now analysed this aspect, eventually under overstimulation conditions, by quenched-flow/cryofixation, combined with electron microscope X-ray microanalysis which registers total calcium concentrations, [Ca]. This allows to follow Ca-signals within a time period (≥30 ms) smaller than one ciliary beat (∼50 ms) and beyond. Particularly under overstimulation conditions (∼10 −5 M Ca 2+ before, 0.5 mM Ca 2+ during stimulation) we find in cilia a [Ca] peak at ∼80 ms and its decay to near-basal levels within 110 ms (90%) to 170 ms (100% decay). This [Ca] wave is followed, with little delay, by a [Ca] wave into subplasmalemmal Ca-stores (alveolar sacs), culminating at ∼100 ms, with a decay to original levels within 170 ms. Also with little delay [Ca] slightly increases in the cytoplasm below. This implies rapid dissipation of Ca 2+ through the ciliary basis, paralleled by a rapid, transient uptake by, and release from cortical stores, suggesting fast exchange mechanisms to be analysed as yet. This novel type of coupling may be relevant for some phenomena described for other cells.

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A plethora of interacting organellar Ca2+ stores

Cited by 84 publications

References 44 publications

Thrombin-mediated increases in cytosolic [Ca²⁺] involve different mechanisms in human pulmonary artery smooth muscle and endothelial cells

Thrombin-mediated increases in cytosolic [Ca²⁺] involve different mechanisms in human pulmonary artery smooth muscle and endothelial cells

Inositol (1,4,5)-Trisphosphate Dynamics and Intracellular Calcium Oscillations in Pancreatic β-Cells

Sub-second calcium coupling between outside medium and subplasmalemmal stores during overstimulation/depolarisation-induced ciliary beat reversal in Paramecium cells

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A plethora of interacting organellar Ca2+ stores

Cited by 84 publications

References 44 publications

Thrombin-mediated increases in cytosolic [Ca2+] involve different mechanisms in human pulmonary artery smooth muscle and endothelial cells

Thrombin-mediated increases in cytosolic [Ca2+] involve different mechanisms in human pulmonary artery smooth muscle and endothelial cells

Inositol (1,4,5)-Trisphosphate Dynamics and Intracellular Calcium Oscillations in Pancreatic β-Cells

Sub-second calcium coupling between outside medium and subplasmalemmal stores during overstimulation/depolarisation-induced ciliary beat reversal in Paramecium cells

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Thrombin-mediated increases in cytosolic [Ca²⁺] involve different mechanisms in human pulmonary artery smooth muscle and endothelial cells

Thrombin-mediated increases in cytosolic [Ca²⁺] involve different mechanisms in human pulmonary artery smooth muscle and endothelial cells