Calcium Oscillations

Dupont, Geneviève; Combettes, Laurent; Bird, Gary S.; Putney, James W.

doi:10.1101/cshperspect.a004226

Cited by 252 publications

(238 citation statements)

References 123 publications

(160 reference statements)

Supporting

Mentioning

214

Contrasting

Order By: Relevance

“…These findings indicate that whereas the 3 distinct InsP 3 R subtypes may all be capable of mediating Ca 2+ oscillations, activators selectively engage specific InsP 3 R subtypes. In addition to InsP 3 R subtype specificity, maintenance of Ca 2+ oscillations is shown to require SOCe (25,32). SOCe requires STIM1, the ER luminal Ca 2+ sensor, which, upon Ca 2+ store depletion, translocates into ER/plasma membrane junctions and couples to activate Orai1 (50) and possibly transient receptor potential channels (TRPCs) (51,52).…”

Section: Store-operated Camentioning

confidence: 99%

“…However, treatment of ECs derived from wild-type mice with LPS triggered Ca 2+ oscillations (Supplemental Figure 3, A, B, and F). Sustained Ca 2+ oscillations operate through the coordinated activation of both storederived Ca 2+ release and store-operated Ca 2+ entry channels (25,32). In non-excitable cells such as ECs, InsP 3 Rs are the major ER Ca 2+ release channels activated by InsP 3 produced when phospholipase C-coupled (PLC-coupled) receptors are activated (33).…”

Section: Ec-specific Stim1mentioning

confidence: 99%

See 1 more Smart Citation

Blockade of NOX2 and STIM1 signaling limits lipopolysaccharide-induced vascular inflammation

Gandhirajan¹,

Meng²,

et al. 2013

View full text Add to dashboard Cite

During sepsis, acute lung injury (ALI) results from activation of innate immune cells and endothelial cells by endotoxins, leading to systemic inflammation through proinflammatory cytokine overproduction, oxidative stress, and intracellular Ca 2+ overload. Despite considerable investigation, the underlying molecular mechanism(s) leading to LPS-induced ALI remain elusive. To determine whether stromal interaction molecule 1-dependent (STIM1-dependent) signaling drives endothelial dysfunction in response to LPS, we investigated oxidative and STIM1 signaling of EC-specific Stim1-knockout mice. Here we report that LPSmediated Ca 2+ oscillations are ablated in ECs deficient in Nox2, Stim1, and type II inositol triphosphate receptor (Itpr2). LPS-induced nuclear factor of activated T cells (NFAT) nuclear accumulation was abrogated by either antioxidant supplementation or Ca 2+ chelation. Moreover, ECs lacking either Nox2 or Stim1 failed to trigger store-operated Ca 2+ entry (SOCe) and NFAT nuclear accumulation. LPS-induced vascular permeability changes were reduced in EC-specific Stim1 -/-mice, despite elevation of systemic cytokine levels. Additionally, inhibition of STIM1 signaling prevented receptor-interacting protein 3-dependent (RIP3-dependent) EC death. Remarkably, BTP2, a small-molecule calcium release-activated calcium (CRAC) channel blocker administered after insult, halted LPS-induced vascular leakage and pulmonary edema. These results indicate that ROS-driven Ca 2+ signaling promotes vascular barrier dysfunction and that the SOCe machinery may provide crucial therapeutic targets to limit sepsis-induced ALI.

show abstract

Section: Store-operated Camentioning

confidence: 99%

Section: Ec-specific Stim1mentioning

confidence: 99%

Blockade of NOX2 and STIM1 signaling limits lipopolysaccharide-induced vascular inflammation

Gandhirajan¹,

Meng²,

et al. 2013

View full text Add to dashboard Cite

show abstract

“…For example, cardiac myocytes require a rapid (hundreds of milliseconds) wholecell calcium transient to trigger contraction every second (Bers 2002), whereas cells that are not electrically excitable typically display calcium oscillations that last for tens of seconds, and can have a periodicity of several minutes, to control gene expression and metabolism (Dupont et al 2011). The rapid calcium signals within myocytes are caused by calcium entering through voltage-activated calcium channels in the plasma membrane, which then triggers calcium release via ryanodine receptors on the sarcoplasmic reticulum.…”

Section: Bootmanmentioning

confidence: 99%

Calcium Signaling

Bootman

2012

Cold Spring Harbor Perspectives in Biology

132

View full text Add to dashboard Cite

“…Endothelial SOCE is mediated by the coupling between the stromal interacting molecule-1 (STIM1), the sensor of ER Ca 2þ depletion, and Orai1, the protein comprising the plasma membrane (PM) channel pore-forming subunit [13,14]. The most suitable pattern for Ca 2þ signaling to drive cell behavior consists in [Ca 2þ ] i oscillations, which embed the molecular information tailored to stimulate specific cellular processes, including cell proliferation and differentiation, via the recruitment of Ca 2þ -sensitive transcription factors, such as NF-jB [15][16][17][18][19]. The composition of the Ca 2þ -signaling tool kit in EPCs is far from being fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

Vascular Endothelial Growth Factor Stimulates Endothelial Colony Forming Cells Proliferation and Tubulogenesis by Inducing Oscillations in Intracellular Ca2+ Concentration

et al. 2011

View full text Add to dashboard Cite

Endothelial progenitor cells (EPCs) home from the bone marrow to the site of tissue regeneration and sustain neovascularization after acute vascular injury and upon the angiogenic switch in solid tumors. Therefore, they represent a suitable tool for cell-based therapy (CBT) in regenerative medicine and provide a novel promising target in the fight against cancer. Intracellular Ca2+ signals regulate numerous endothelial functions, such as proliferation and tubulogenesis. The growth of endothelial colony forming cells (ECFCs), which are EPCs capable of acquiring a mature endothelial phenotype, is governed by store-dependent Ca2+ entry (SOCE). This study aimed at investigating the nature and the role of VEGF-elicited Ca2+ signals in ECFCs. VEGF induced asynchronous Ca2+ oscillations, whose latency, amplitude, and frequency were correlated to the growth factor dose. Removal of external Ca2+ (0Ca2+) and SOCE inhibition with N-(4-[3,5-bis(trifluoromethyl)-1H-pyrazol-1-yl]phenyl)-4-methyl-1,2,3-thiadiazole-5-carboxamide (BTP-2) reduced the duration of the oscillatory signal. Blockade of phospholipase C-γ with U73122, emptying the inositol-1,4,5-trisphosphate (InsP3)-sensitive Ca2+ pools with cyclopiazonic acid (CPA), and inhibition of InsP3 receptors with 2-APB prevented the Ca2+ response to VEGF. VEGF-induced ECFC proliferation and tubulogenesis were inhibited by the Ca2+-chelant, BAPTA, and BTP-2. NF-κB activation by VEGF was impaired by BAPTA, BTP-2, and its selective blocker, thymoquinone. Thymoquinone, in turn, suppressed VEGF-dependent ECFC proliferation and tubulogenesis. These data indicate that VEGF-induced Ca2+ oscillations require the interplay between InsP3-dependent Ca2+ release and SOCE, and promote ECFC growth and tubulogenesis by engaging NF-κB. This novel signaling pathway might be exploited to enhance the outcome of CBT and chemotherapy.

show abstract

Calcium Oscillations

Cited by 252 publications

References 123 publications

Blockade of NOX2 and STIM1 signaling limits lipopolysaccharide-induced vascular inflammation

Blockade of NOX2 and STIM1 signaling limits lipopolysaccharide-induced vascular inflammation

Calcium Signaling

Vascular Endothelial Growth Factor Stimulates Endothelial Colony Forming Cells Proliferation and Tubulogenesis by Inducing Oscillations in Intracellular Ca2+ Concentration

Contact Info

Product

Resources

About