Differential sensitivity to nickel and SK&amp;F96365 of second messengerm operated and receptormoperated calcium channels in rat submandibular ductal cells

Chaib, Naima; Kabré, Elie; Metioui, Mourad; Alzola, Eduardo; Dantinne, C; Marino, Aída; Dehaye, Jean-Paul

doi:10.1016/s0143-4160(98)90096-3

Cited by 19 publications

(12 citation statements)

References 36 publications

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“…1d). Furthermore, the nonspecific Ca 2ϩ channel antagonist, Ni 2ϩ , which inhibits SOC at higher concentrations (20), suppressed sperm accumulation at 5 mM (Fig. 1e).…”

Section: Resultsmentioning

confidence: 88%

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Store-operated calcium channel regulates the chemotactic behavior of ascidian sperm

Yoshida

Ishikawa

Izumi

et al. 2002

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

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The sperm-activating and -attracting factor released from the eggs of the ascidians Ciona intestinalis and Ciona savignyi requires extracellular Ca 2؉ for activating sperm motility and eliciting chemotactic behavior of the activated sperm toward the egg. Here, we show that modulators of the store-operated Ca 2؉ channel, SK&F96365, Ni 2؉ , 2-aminoethoxydiphenylborane, and thapsigargin inhibit the chemotactic behavior of the ascidian sperm; on the other hand, blockers of voltage-dependent Ca 2؉ channels did not inhibit the chemotaxis, even though they inhibited the sperm activation operated by voltage-dependent Ca 2؉ channels. The blockers of store-operated Ca 2؉ channels also inhibited the asymmetrical flagellar beating and turning movements of the ascidian sperm, which are typical signs of sperm chemotaxis. Depletion of internal Ca 2؉ stores by thapsigargin induced capacitative Ca 2؉ entry into the sperm, which was blocked by SK&F96365. These results suggest that the intracellular Ca 2؉ concentration increase through the store-operated Ca 2؉ channels induces asymmetrical flagellar movements to establish the chemotactic behavior of the sperm. I t is now well known that many cells, e.g., leukocytes, starved amoebae of Dictyostelium discoideum, bacteria, and migrating axon cells during development, can detect an extracellular chemical gradient and migrate toward the source of the chemicals, that is, exhibit chemotactic behavior. There is a variety of factors inducing chemotaxis of cells, e.g., food, pathogens, partner cells, etc., and chemotactic behavior of cells is one of the important communication systems between separated cells. Chemotactic behavior of the sperm toward an egg during fertilization in animal species is a typical case, first reported in hydrozoans (1). This phenomenon is now widely known to occur, from sponges to humans (2-4), and much effort has been devoted to clarifying the mechanisms underlying sperm chemotaxis.Extracellular Ca 2ϩ is generally accepted as being an important factor in the induction of chemotactic behavior of sperm in many plant and animal species (5-8). In the case of the sea urchin, Arbacia punctulata, a peptide named resact in the jelly layer of the egg has been shown to have sperm-activating and -attracting activities (7). The peptide increases the intracellular Ca 2ϩ concentration ([Ca 2ϩ ] i ) via cAMP-gated Ca 2ϩ channels (9, 10), which, in turn, induces asymmetrical flagellum movements (5, 11, 12) that result in reorientation of the sperm swimming direction (13). The role of extracellular Ca 2ϩ -induced asymmetrical flagellar movement in inducing sperm chemotaxis has also been reported in hydrozoan species (14). Ascidian sperm chemotactic behavior is also characterized by abrupt turning movements of the sperm (15, 16). Furthermore, it has been shown that the sperm-attracting activity in the ascidians Ciona intestinalis and Ciona savignyi does not originate from the overall surface of the egg coats, such as follicle cells, but from the vegetal pole of the egg (17). We al...

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“…1d). Furthermore, the nonspecific Ca 2ϩ channel antagonist, Ni 2ϩ , which inhibits SOC at higher concentrations (20), suppressed sperm accumulation at 5 mM (Fig. 1e).…”

Section: Resultsmentioning

confidence: 88%

“…SK&F96365, a blocker of receptor-and store-operated Ca 2ϩ channels (SOC) (20), inhibited the chemotaxis of C. intestinalis sperm: 1 M or more SK&F96365 prevented accumulation of sperm around the capillary tip, in both the presence and absence of extracellular Ca 2ϩ (Fig. 1d).…”

Section: Resultsmentioning

confidence: 95%

Store-operated calcium channel regulates the chemotactic behavior of ascidian sperm

Yoshida

Ishikawa

Izumi

et al. 2002

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

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“…However, it has been in turn classified as a specific blocker of store-operated channels [47,106], of non-store-operated ones [105,106], or as a non-specific blocker, acting also on VOCs [8,105]. Moreover, other aspecific effects have been reported, both of activation and block of other types of channels [89,108].…”

Section: Skandf 96365mentioning

confidence: 99%

Intracellular Calcium, Endothelial Cells and Angiogenesis

Munaron

2006

PRA

124

117

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The proliferation and motility of vascular endothelial cells (ECs) are critical steps in angiogenesis and are strictly controlled by different extracellular signals. Among mitogens, peptides binding to tyrosine kinase receptors (i.e. VEGFs and FGFs) are well known and are released by several cell types, including ECs and tumor cells. The binding of mitogens to their specific receptors triggers intracellular signaling cascades, involving a number of messengers working in a sort of network. In particular, in this review we describe the increases of calcium levels in the cytosol, a universal, evolutionary conserved and highly versatile signal involved in the regulation of EC's proliferation and motility. Most mitogens, including angiogenic factors, generate cytosolic calcium rises through two mechanisms: entry from extracellular medium, through the opening of calcium permeable channels in the plasma membrane, or release from intracellular organelles (mainly endoplasmic reticulum, ER). Calcium entry, the main topic of this review, can be dependent on previously IP(3)-activated emptying of calcium stores (store-dependent or capacitative calcium entry--CCE), or independent on it (non capacitative calcium entry, NCCE). The intracellular pathways underlying calcium entry are under investigation and recently arachidonic acid (AA) and nitric oxide (NO) metabolism have been suggested to play a key role, at least in some cell types. Even if some calcium entry blockers are under clinical trial with encouraging results, a better knowledge about the molecular nature of calcium channels and their intracellular regulation, together with a more detailed description of spatiotemporal dynamics of intracellular calcium events, could lead to new and more specific strategies in therapeutical approach to cancer progression and angiogenesis.

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“…2-APB and SKF96365 inhibit SOCE in salivary gland cells [1], [52], [53], [54] and blocked increases in ERK1/2 phosphorylation by TG and carbachol to a varying degree. Of note, ARC channels are not sensitive to 2-APB [55].…”

Section: Discussionmentioning

confidence: 92%

Activation of ERK1/2 by Store-Operated Calcium Entry in Rat Parotid Acinar Cells

Soltoff

Lannon

2013

PLoS ONE

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The regulation of intracellular Ca2+ concentration ([Ca2+]i) plays a critical role in a variety of cellular processes, including transcription, protein activation, vesicle trafficking, and ion movement across epithelial cells. In many cells, the activation of phospholipase C-coupled receptors hydrolyzes membrane phosphoinositides and produces the depletion of endoplasmic reticulum Ca2+ stores, followed by the sustained elevation of [Ca2+]i from Ca2+ entry across the plasma membrane via store-operated Ca2+ entry (SOCE). Ca2+ entry is also increased in a store-independent manner by arachidonate-regulated Ca2+ (ARC) channels. Using rat parotid salivary gland cells, we examined multiple pathways of Ca2+ entry/elevation to determine if they activated cell signaling proteins and whether this occurred in a pathway-dependent manner. We observed that SOCE activates extracellular signal-related kinases 1 and 2 (ERK1/2) to ∼3-times basal levels via a receptor-independent mechanism when SOCE was initiated by depleting Ca2+ stores using the endoplasmic reticulum Ca2+-ATPase inhibitor thapsigargin (TG). TG-initiated ERK1/2 phosphorylation increased as rapidly as that initiated by the muscarinic receptor agonist carbachol, which promoted an increase to ∼5-times basal levels. Notably, ERK1/2 phosphorylation was not increased by the global elevation of [Ca2+]i by Ca2+ ionophore or by Ca2+ entry via ARC channels in native cells, although ERK1/2 phosphorylation was increased by Ca2+ ionophore in Par-C10 and HSY salivary cell lines. Agents and conditions that blocked SOCE in native cells, including 2-aminoethyldiphenyl borate (2-APB), SKF96363, and removal of extracellular Ca2+, also reduced TG- and carbachol-stimulated ERK1/2 phosphorylation. TG-promoted ERK1/2 phosphorylation was blocked when SRC and Protein Kinases C (PKC) were inhibited, and it was blocked in cells pretreated with β-adrenergic agonist isoproterenol. These observations demonstrate that ERK1/2 is activated by a selective mechanism of Ca2+ entry (SOCE) in these cells, and suggest that ERK1/2 may contribute to events downstream of SOCE.

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Differential sensitivity to nickel and SK&F96365 of second messengerm operated and receptormoperated calcium channels in rat submandibular ductal cells

Cited by 19 publications

References 36 publications

Store-operated calcium channel regulates the chemotactic behavior of ascidian sperm

Store-operated calcium channel regulates the chemotactic behavior of ascidian sperm

Intracellular Calcium, Endothelial Cells and Angiogenesis

Activation of ERK1/2 by Store-Operated Calcium Entry in Rat Parotid Acinar Cells

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