Cyclopiazonic Acid-Induced Ca2+ Store Depletion Initiates Endothelium-Dependent Hyperpolarization-Mediated Vasorelaxation of Mesenteric Arteries in Healthy and Colitis Mice

Zhang, Lu Yun; Chen, Xiong Ying; Dong, Hui; Xu, Feng

doi:10.3389/fphys.2021.639857

Cited by 7 publications

(8 citation statements)

References 47 publications

(57 reference statements)

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“…Animal studies addressing EDH-mediated relaxations revealed a well-defined production of cyclooxygenases and NO synthase inhibitors that are coupled with hyperpolarization of VSMCs located in the proximity of these molecular reactions. Some experimental studies have established the heterogeneous nature of EDH factors by reporting the specific characteristics relating to the different species and vascular beds of concern [ 53 , 54 , 55 ]. Greater production of epoxyeicosatrienoic acids, which constitute the fundamental metabolites of the arachidonic P450 epoxygenase sequential reactions were noted [ 56 , 57 , 58 , 59 , 60 ].…”

Section: Resultsmentioning

confidence: 99%

Pathophysiology and Outcomes of Endothelium Function in Coronary Microvascular Diseases: A Systematic Review of Randomized Controlled Trials and Multicenter Study

Singh

Nappi

2022

Biomedicines

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Background: Coronary macrovascular disease is a concept that has been well-studied within the literature and has long been the subject of debates surrounding coronary artery bypass grafting (CABG) vs. Percutaneous Coronary Intervention (PCI). ISCHEMIA trial reported no statistical difference in the primary clinical endpoint between initial invasive management and initial conservative management, while in the ORBITA trial PCI did not improve angina frequency score significantly more than placebo, albeit PCI resulted in more patient-reported freedom from angina than placebo. However, these results did not prove the superiority of the PCI against OMT, therefore do not indicate the benefit of PCI vs. the OMT. Please rephrase the sentence. We reviewed the role of different factors responsible for endothelial dysfunction from recent randomized clinical trials (RCTs) and multicentre studies. Methods: A detailed search strategy was performed using a dataset that has previously been published. Data of pooled analysis include research articles (human and animal models), CABG, and PCI randomized controlled trials (RCTs). Details of the search strategy and the methods used for data pooling have been published previously and registered with Open-Source Framework. Results: The roles of nitric oxide (NO), endothelium-derived contracting factors (EDCFs), and vasodilator prostaglandins (e.g., prostacyclin), as well as endothelium-dependent hyperpolarization (EDH) factors, are crucial for the maintenance of vasomotor tone within the coronary vasculature. These homeostatic mechanisms are affected by sheer forces and other several factors that are currently being studied, such as vaping. The role of intracoronary testing is crucial when determining the effects of therapeutic medications with further studies on the horizon. Conclusion: The true impact of coronary microvascular dysfunction (CMD) is perhaps underappreciated, which supports the role of medical therapy in determining outcomes. Ongoing trials are underway to further investigate the role of therapeutic agents in secondary prevention.

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Section: Resultsmentioning

confidence: 99%

Pathophysiology and Outcomes of Endothelium Function in Coronary Microvascular Diseases: A Systematic Review of Randomized Controlled Trials and Multicenter Study

Singh

Nappi

2022

Biomedicines

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“…This decrease in stem cell population was observed with concentrations of SKF-96365 and YM-58483 that have been used to block the physiological effects of SOC [ 31 , 46 , 47 , 48 , 49 ]. As SKF-96365 and YM-58483 may also target other receptor channels (ROC), GSK-7975A, a more specific inhibitor of Orai-dependent SOCE was used [ 50 , 51 , 52 ]. The fact that GSK-7975A had also significant effects on GSC supports the idea that SOC play a key role in maintaining the GSC pool in GBM as they do in oral/oropharyngeal squamous cell carcinoma cancer stem cells and in liver cancer stem cells [ 53 , 54 ].…”

Section: Discussionmentioning

confidence: 99%

Store-Operated Calcium Channels Control Proliferation and Self-Renewal of Cancer Stem Cells from Glioblastoma

Terrié

Déliot

Benzidane

et al. 2021

Cancers

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Glioblastoma is the most frequent and deadly form of primary brain tumors. Despite multimodal treatment, more than 90% of patients experience tumor recurrence. Glioblastoma contains a small population of cells, called glioblastoma stem cells (GSC) that are highly resistant to treatment and endowed with the ability to regenerate the tumor, which accounts for tumor recurrence. Transcriptomic studies disclosed an enrichment of calcium (Ca2+) signaling transcripts in GSC. In non-excitable cells, store-operated channels (SOC) represent a major route of Ca2+ influx. As SOC regulate the self-renewal of adult neural stem cells that are possible cells of origin of GSC, we analyzed the roles of SOC in cultures of GSC previously derived from five different glioblastoma surgical specimens. Immunoblotting and immunocytochemistry experiments showed that GSC express Orai1 and TRPC1, two core SOC proteins, along with their activator STIM1. Ca2+ imaging demonstrated that SOC support Ca2+ entries in GSC. Pharmacological inhibition of SOC-dependent Ca2+ entries decreased proliferation, impaired self-renewal, and reduced expression of the stem cell marker SOX2 in GSC. Our data showing the ability of SOC inhibitors to impede GSC self-renewal paves the way for a strategy to target the cells considered responsible for conveying resistance to treatment and tumor relapse.

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“…SOCE can also be activated by the pharmacological depletion of the ER Ca 2+ by means of multiple drugs. The most common strategy to evoke SOCE in endothelial cells (and in circulating ECFCs) is represented by the blockade of Sarco-Endoplasmic Reticulum Ca 2+ (SERCA) activity with cyclopiazonic acid (CPA) [ 61 , 62 , 63 , 64 ], a mycotoxin and a fungal neurotoxin produced by the moulds Aspergillus and Penicillium and by thapsigargin [ 38 , 39 , 51 , 63 ], a plant-derived lactone, whereas 2,5-di-tert-butylhydroquinone (tBHQ) was mostly exploited in earlier studies [ 65 , 66 , 67 ]. The blockade of SERCA activity results in passive ER Ca 2+ efflux from leakage channels, whose molecular identity in endothelial cells remains to be unveiled [ 68 ].…”

Section: How To Activate Endothelial Soce: Physiological Vs Pharmacol...mentioning

confidence: 99%

The Molecular Heterogeneity of Store-Operated Ca2+ Entry in Vascular Endothelial Cells: The Different roles of Orai1 and TRPC1/TRPC4 Channels in the Transition from Ca2+-Selective to Non-Selective Cation Currents

Moccia

Brunetti

Perna

et al. 2023

IJMS

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Store-operated Ca2+ entry (SOCE) is activated in response to the inositol-1,4,5-trisphosphate (InsP3)-dependent depletion of the endoplasmic reticulum (ER) Ca2+ store and represents a ubiquitous mode of Ca2+ influx. In vascular endothelial cells, SOCE regulates a plethora of functions that maintain cardiovascular homeostasis, such as angiogenesis, vascular tone, vascular permeability, platelet aggregation, and monocyte adhesion. The molecular mechanisms responsible for SOCE activation in vascular endothelial cells have engendered a long-lasting controversy. Traditionally, it has been assumed that the endothelial SOCE is mediated by two distinct ion channel signalplexes, i.e., STIM1/Orai1 and STIM1/Transient Receptor Potential Canonical 1(TRPC1)/TRPC4. However, recent evidence has shown that Orai1 can assemble with TRPC1 and TRPC4 to form a non-selective cation channel with intermediate electrophysiological features. Herein, we aim at bringing order to the distinct mechanisms that mediate endothelial SOCE in the vascular tree from multiple species (e.g., human, mouse, rat, and bovine). We propose that three distinct currents can mediate SOCE in vascular endothelial cells: (1) the Ca2+-selective Ca2+-release activated Ca2+ current (ICRAC), which is mediated by STIM1 and Orai1; (2) the store-operated non-selective current (ISOC), which is mediated by STIM1, TRPC1, and TRPC4; and (3) the moderately Ca2+-selective, ICRAC-like current, which is mediated by STIM1, TRPC1, TRPC4, and Orai1.

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Cyclopiazonic Acid-Induced Ca2+ Store Depletion Initiates Endothelium-Dependent Hyperpolarization-Mediated Vasorelaxation of Mesenteric Arteries in Healthy and Colitis Mice

Cited by 7 publications

References 47 publications

Pathophysiology and Outcomes of Endothelium Function in Coronary Microvascular Diseases: A Systematic Review of Randomized Controlled Trials and Multicenter Study

Pathophysiology and Outcomes of Endothelium Function in Coronary Microvascular Diseases: A Systematic Review of Randomized Controlled Trials and Multicenter Study

Store-Operated Calcium Channels Control Proliferation and Self-Renewal of Cancer Stem Cells from Glioblastoma

The Molecular Heterogeneity of Store-Operated Ca2+ Entry in Vascular Endothelial Cells: The Different roles of Orai1 and TRPC1/TRPC4 Channels in the Transition from Ca2+-Selective to Non-Selective Cation Currents

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