IP3 receptor subtype-dependent activation of store-operated calcium entry through ICRAC

Peinelt, Christine; Beck, Andreas; Monteilh-Zoller, Mahealani K.; Penner, Reinhold; Fleig, Andrea

doi:10.1016/j.ceca.2008.12.001

Cited by 17 publications

(16 citation statements)

References 33 publications

(39 reference statements)

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“…5B). However, the DT40 KO cells have previously been shown to activate endogenous I CRAC when stores are depleted independent of IP 3 receptors [40]. To confirm these previous observations we applied 10 µM thapsigargin (Tg) at 60 s resulting in I CRAC development (Fig.…”

Section: Resultssupporting

confidence: 57%

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Activation of store-operated ICRAC by hydrogen peroxide

et al. 2010

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SUMMARYReactive oxygen species such as hydrogen peroxide (H 2 O 2 ) play a role in both innate immunity as well as cellular injury. H 2 O 2 induces changes in intracellular calcium ([Ca 2+ ] i ) in many cell types and this seems to be at least partially mediated by transient receptor potential melastatin 2 (TRPM2) in cells that express this channel. Here we show that low concentrations of H 2 O 2 induce the activation of the Ca 2+ -release activated Ca 2+ current I CRAC . This effect is not mediated by direct CRAC channel activation, since H 2 O 2 does not activate heterologously expressed CRAC channels independently of stromal interaction molecule (STIM). Instead, I CRAC activation is partially mediated by store depletion through activation of inositol 1,4,5 trisphosphate receptors (IP 3 R), since pharmacological inhibition of IP 3 receptors by heparin or molecular knock-out of all IP 3 receptors in DT40 B cells strongly reduce H 2 O 2 -induced I CRAC . The remainder of H 2 O 2 -induced I CRAC activation is likely mediated by IP 3 R-independent store-depletion. Our data suggest that H 2 O 2 can activate Ca 2+ entry through TRPM2 as well as store-operated CRAC channels, thereby adding a new facet to ROSinduced Ca 2+ signaling.

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Section: Resultssupporting

confidence: 57%

“…As DT40 cells develop very small I CRAC , we optimized experimental conditions by increasing the external CaCl 2 concentration to 20 mM and expanding the voltage ramp to −150 mV, extracting current amplitudes at −130 mV [40]. Furthermore internal MgCl 2 concentration was increased to 3 mM to inhibit endogenous TRPM7 currents.…”

Section: Resultsmentioning

confidence: 99%

Activation of store-operated ICRAC by hydrogen peroxide

et al. 2010

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“…According to this model, that has been supported by convincing experimental data in a number of cell types [see 90, for a recent review], only ATP engages the Ca 2+ storage site which lies in close apposition to the PM in ECFCs [25]. In this view, it has been shown that InsP 3 R-2 and InsP 3 R-3, but not InsP 3 R1, drive SOCE activation in avian B cells [93], while InsP 3 R-1 is the main isoform linked to Stim1 translocation in H4IIE liver cells [94]. ECFCs express all the three known InsP 3 R subtypes: future work will have to assess which of them is selectively coupled to SOCE in these cells.…”

Section: Store-operated Ca 2+ Entry In Endothelial Colony Forming Celmentioning

confidence: 72%

Store-Dependent Ca2+ Entry in Endothelial Progenitor Cells As a Perspective Tool to Enhance Cell-Based Therapy and Adverse Tumour Vascularization

Moccia

Dragoni

Lodola

et al. 2012

CMC

108

152

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Endothelial progenitor cells (EPCs) have recently been employed in cell-based therapy (CBT) to promote neovascularization and regeneration of ischemic organs, such as heart and limbs. Furthermore, EPCs may be recruited from bone marrow by growing tumors to drive the angiogenic switch through physical engrafting into the lumen of nascent vessels or paracrine release of pro-angiogenic factors. CBT is hampered by the paucity of EPCs harvested from peripheral blood and suffered from several pitfalls, including the differentiation outcome of transplanted cells and low percentage of engrafted cells. Therefore, CBT will benefit from a better understanding of the signal transduction pathway(s) which govern(s) EPC homing, proliferation and incorporation into injured tissues. At the same time, this information might outline alternative molecular targets to combat tumoral neovascularization. We have recently found that store-operated Ca(2+) entry, a Ca(2+)-permeable membrane pathway that is activated upon depletion of the inositol-1,4,5-trisphosphate-sensitive Ca(2+) pool, is recruited by vascular endothelial growth factor to support proliferation and tubulogenesis in human circulating endothelial colony forming cells (ECFCs). ECFCs are a subgroup of EPCs that circulate in the peripheral blood of adult individuals and are able to proliferate and differentiate into endothelial cells and form capillary networks in vitro and contribute to neovessel formation in vivo. The present review will discuss the relevance of SOCE to ECFC-based cell therapy and will address the pharmacological inhibition of store-dependent Ca(2+) channels as a promising target for anti-angiogenic treatments.

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“…Outside the immune system, these cells include (but are not limited to) vascular endothelial (88–90) and smooth muscle cells (91, 92), pancreatic acinar cells (93), hepatocytes (94), and adrenal chromaffine cells (95). In the immune system, SOCE and I CRAC have been observed in many different cell types of the lymphoid and myeloid lineage such as T cells (3), mast cells (4), B cells (96–98), dendritic cells (12), macrophages (99), NK cells (100), and neutrophils (11). It is likely that SOCE plays a role in other cell types in the immune system as well and contributes to proper innate and adaptive immune responses.…”

Section: Stim and Orai Expression In Cells Of The Immune Systemmentioning

confidence: 99%

ORAI1 and STIM1 deficiency in human and mice: roles of store‐operated Ca²⁺ entry in the immune system and beyond

Feske¹

2009

Immunological Reviews

266

298

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Store-operated Ca2+ entry (SOCE) is a mechanism used by many cells types including lymphocytes and other immune cells to increase intracellular Ca2+ concentrations to initiate signal transduction. Activation of immunoreceptors such as the T-cell receptor, B-cell receptor, or Fc receptors results in the release of Ca2+ ions from endoplasmic reticulum (ER) Ca2+ stores and subsequent activation of plasma membrane Ca2+ channels such as the well-characterized Ca2+ release-activated Ca2+ (CRAC) channel. Two genes have been identified that are essential for SOCE: ORAI1 as the pore-forming subunit of the CRAC channel in the plasma membrane and stromal interaction molecule-1 (STIM1) sensing the ER Ca2+ concentration and activating ORAI1-CRAC channels. Intense efforts in the past several years have focused on understanding the molecular mechanism of SOCE and the role it plays for cell functions in vitro and in vivo. A number of transgenic mouse models have been generated to investigate the role of ORAI1 and STIM1 in immunity. In addition, mutations in ORAI1 and STIM1 identified in immunodeficient patients provide valuable insight into the role of both genes and SOCE. This review focuses on the role of ORAI1 and STIM1 in vivo, discussing the phenotypes of ORAI1- and STIM1-deficient human patients and mice.

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IP3 receptor subtype-dependent activation of store-operated calcium entry through ICRAC

Cited by 17 publications

References 33 publications

Activation of store-operated ICRAC by hydrogen peroxide

Activation of store-operated ICRAC by hydrogen peroxide

Store-Dependent Ca2+ Entry in Endothelial Progenitor Cells As a Perspective Tool to Enhance Cell-Based Therapy and Adverse Tumour Vascularization

ORAI1 and STIM1 deficiency in human and mice: roles of store‐operated Ca²⁺ entry in the immune system and beyond

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IP3 receptor subtype-dependent activation of store-operated calcium entry through ICRAC

Cited by 17 publications

References 33 publications

Activation of store-operated ICRAC by hydrogen peroxide

Activation of store-operated ICRAC by hydrogen peroxide

Store-Dependent Ca2+ Entry in Endothelial Progenitor Cells As a Perspective Tool to Enhance Cell-Based Therapy and Adverse Tumour Vascularization

ORAI1 and STIM1 deficiency in human and mice: roles of store‐operated Ca2+ entry in the immune system and beyond

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ORAI1 and STIM1 deficiency in human and mice: roles of store‐operated Ca²⁺ entry in the immune system and beyond