Capacitative Calcium Entry

Putney, Jr. James W.

doi:10.1007/978-1-4684-6471-9

Cited by 183 publications

(95 citation statements)

References 10 publications

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“…In a cellular context, the onset of Ca 2+ signaling is marked by increase in cytosolic Ca 2+ both by release of Ca 2+ from intracellular endoplasmic reticulum (ER) stores as well as influx across the plasma membrane (PM) [23]. This increase in intracellular Ca 2+ triggers activation of downstream signaling pathways leading to inflammatory response [24]. The regulation of calcium signaling by parasites may be a novel immune suppressive mechanism to block the initiation of the inflammatory pathway.…”

Section: Introductionmentioning

confidence: 99%

Helminth Induced Suppression of Macrophage Activation Is Correlated with Inhibition of Calcium Channel Activity

et al. 2014

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Helminth parasites cause persistent infections in humans and yet many infected individuals are asymptomatic. Neurocysticercosis (NCC), a disease of the central nervous system (CNS) caused by the cestode Taenia solium, has a long asymptomatic phase correlated with an absence of brain inflammation. However, the mechanisms of immune suppression remain poorly understood. Here we report that murine NCC displays a lack of cell surface maturation markers in infiltrating myeloid cells. Furthermore, soluble parasite ligands (PL) failed to induce maturation of macrophages, and inhibited TLR-induced inflammatory cytokine production. Importantly, PL treatment abolished both LPS and thapsigargin-induced store operated Ca2+ entry (SOCE). Moreover, electrophysiological recordings demonstrated PL-mediated inhibition of LPS or Tg-induced currents that were TRPC1-dependent. Concomitantly STIM1-TRPC1 complex was also impaired that was essential for SOCE and sustained Ca2+ entry. Likewise loss of SOCE due to PL further inhibited NFkB activation. Overall, our results indicate that the negative regulation of agonist induced Ca2+ signaling pathway by parasite ligands may be a novel immune suppressive mechanism to block the initiation of the inflammatory response associated with helminth infections.

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Section: Introductionmentioning

confidence: 99%

Helminth Induced Suppression of Macrophage Activation Is Correlated with Inhibition of Calcium Channel Activity

et al. 2014

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“…Recent studies have demonstrated that intracellular Ca 2+ elevation which is caused by binding of inositol triphosphate (IP 3 ) and IP 3 receptor on the endoplasmic reticulum membrane participates in the regulation of immune cell maturation including proliferation through activation of calcium dependent-protein kinase (Jun and Goodnow, 2003). In addition, PKC activated by diacyl glycerol (DAG), which is another phosphatidyl inositol 4,5 bisphosphate (PIP 2 ) metabolite through PLC activation, is critical role in proliferation and differentiation of various cell types including in B lymphocytes (Putney et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Cudrania tricupidataBureau (CTB) Glycoprotein Inhibits Proliferation by Di(2-ethylhexyl) phthalate in Primary Splenocytes: Responses in Cell Proliferation Signaling

Lim

2011

Immunological Investigations

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The aim of the present study was to evaluate inhibitory effect of CTB glycoprotein isolated from Cudrania tricuspidata Bureau on DEHP-induced cell proliferation in lymphocytes. Our results revealed that DEHP increased lymphocyte proliferation as confirmed by increasing [(3)H]thymidine incorporation, and proliferating cell nuclear antigen (PCNA), cyclin D1, and cyclin-dependent kinase (CDK)-4 expression. This was accompanied by induced intracellular Ca(2+) level, protein kinase C (PKC) translocation from cytosol to membrane, ERK1/2 phosphorylation, and nuclear factor (NF)-κB transcriptional activation in DEHP-treated cells. However, CTB glycoprotein (100 μg/ml) reduced labeled thymidine incorporation and PCNA expression in DEHP-treated cells. Additionally CTB glycoprotein reduced Ca(2+) level, PKC translocation, ERK1/2 phosphorylation, NF-κB transcriptional activation, cell cycle proteins (cyclin D1 and CDK4) expression in cells. The activation of NF-κB was collectively blocked by pretreatment with PKC inhibitor (staurosporine) and ERK1/2 inhibitor (PD98059), respectively. The results from these experiments indicate that CTB glycoprotein inhibits cell proliferation via down regulations of Ca(2+)/PKC, ERK1/2, and cell cycle proteins induced by DEHP. Therefore, we suggest that the CTB glycoprotein might be one component for prevention of cell proliferation-related immune diseases.

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“…IP 3 R is activated by the presence of cytoplasmic IP 3 , a product generated by several different types of PLC signaling pathways that are predominantly linked to surface receptor activation on the plasma membrane. RyR, on the other hand, is activated by the calcium influx associated with pathologic increases of the ion, a mechanism known as calcium-induced calcium release (CICR) [59] or 232 Intracellular Calcium Signaling capacitative entry [60], a process involving the opening of plasma membrane calcium channels as mentioned earlier. Furthermore, other isoforms of RyR are also triggered by cyclic adenosine diphosphate ribose (cADPR), a vital component in signal transduction through cell-permeant gaseous messengers, such as NO, or metabolic factors, such as ROS produced during I/R injury.…”

Section: Endoplasmic Reticulum (Er)mentioning

confidence: 99%

“…The mechanism of regulated calcium entry in nonexcitable cells is through a process known as capacitative calcium entry or store-operated calcium entry, in which the depletion of intracellular calcium stores, due to the action of inositol triphosphate (IP 3 ) or other calciumreleasing signals, activates a signaling pathway leading to the opening of plasma membrane calcium channels [31] ( Figure 1). …”

Section: Intracellular Calcium Signalingmentioning

confidence: 99%

Intracellular Calcium Signaling Pathways during Liver Ischemia and Reperfusion

Chang

Chehab

Kink

et al. 2010

Journal of Investigative Surgery

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Calcium plays a major role in intracellular signaling mechanisms during ischemia reperfusion (I/R) injury of a liver cell. Under ischemic conditions, the absence of oxygen arrests oxidative phosphorylation, thereby eliminating the energy source by which hepatocellular mechanisms maintain homeostasis of calcium. This, in turn, leaves nonselective plasma membrane influx pores unopposed and results in a net increase in intracellular calcium concentrations. Subsequent reperfusion marks the onset and progression of apoptosis and necrosis, as it involves inflammatory responses as well as free-radical formation due to re-oxygenation of cells. These processes destroy the structural integrity of organelles, leading to disruptive redistribution of calcium between cellular and subcellular compartments. This initial elevation and later imbalance of intracellular calcium concentrations associated with I/R induce various molecular responses within each organelle. In the cytoplasm, a series of pro-apoptotic pathways involving various calcium sensitive enzymes are activated. The injury is further exacerbated in the endoplasmic reticulum (ER) due to the malfunction of mechanisms responsible for intracellular calcium sequestration. Both the mitochondria and the nucleus are also adversely affected, as their structural integrity and physiologic functions are disrupted. To date, however, the precise pathophysiology of these calcium-mediated signaling pathways is not fully understood due to its complex nature. This review aims to systematically examine the current literature about individual molecular signaling pathways in the cytoplasm, ER, mitochondria, and the nucleus prior to causing time-sensitive progression of permanent tissue injury.

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Capacitative Calcium Entry

Cited by 183 publications

References 10 publications

Helminth Induced Suppression of Macrophage Activation Is Correlated with Inhibition of Calcium Channel Activity

Helminth Induced Suppression of Macrophage Activation Is Correlated with Inhibition of Calcium Channel Activity

Cudrania tricupidataBureau (CTB) Glycoprotein Inhibits Proliferation by Di(2-ethylhexyl) phthalate in Primary Splenocytes: Responses in Cell Proliferation Signaling

Intracellular Calcium Signaling Pathways during Liver Ischemia and Reperfusion

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