Calcium regulation in aortic smooth muscle cells during the initial phase of tunicamycin-induced endo/sarcoplasmic reticulum stress

Ziomek, Gabriela; Zanjani, Parisa Cheraghi; Arman, Darian; Breemen, Cornelis van; Esfandiarei, Mitra

doi:10.1016/j.ejphar.2014.04.025

Cited by 8 publications

(6 citation statements)

References 40 publications

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“…SOCE directly or indirectly regulates the Ca 2+ -dependent UPR [1314]. Tunicamycin has been shown to increase intracellular Ca 2+ concentration in lymphoid and smooth muscle cells by SOCE [1516], but the specific calcium channel was not determined.…”

Section: Discussionmentioning

confidence: 99%

“…Celine et al reported that CHOP-10, an UPR-related protein, transcriptionally repressed eNOS by modulating the activity of eNOS gene promoter [28]. However, Ziomek et al [16] found that tunicamycin induced a significant increase of intracellular Ca 2+ in vascular smooth muscle cells, but it was dependent on the direct permeability of the plasma membrane, ER, and sarcoplasmic reticulum to calcium, not on the activation of calcium channels. This difference may be a consequence to the different cell types that were used.…”

Section: Discussionmentioning

confidence: 99%

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Involvement of Orai1 in tunicamycin-induced endothelial dysfunction

Yang

Xue

Kuang

et al. 2019

Korean J Physiol Pharmacol

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Endoplasmic reticulum (ER) stress is mediated by disturbance of Ca 2+ homeostasis. The store-operated calcium (SOC) channel is the primary Ca 2+ channel in non-excitable cells, but its participation in agent-induced ER stress is not clear. In this study, the effects of tunicamycin on Ca 2+ influx in human umbilical vein endothelial cells (HUVECs) were observed with the fluorescent probe Fluo-4 AM. The effect of tunicamycin on the expression of the unfolded protein response (UPR)-related proteins BiP and CHOP was assayed by western blotting with or without inhibition of Orai1. Tunicamycin induced endothelial dysfunction by activating ER stress. Orai1 expression and the influx of extracellular Ca 2+ in HUVECs were both upregulated during ER stress. The SOC channel inhibitor SKF96365 reversed tunicamycin-induced endothelial cell dysfunction by inhibiting ER stress. Regulation of tunicamycin-induced ER stress by Orai1 indicates that modification of Orai1 activity may have therapeutic value for conditions with ER stress-induced endothelial dysfunction.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Involvement of Orai1 in tunicamycin-induced endothelial dysfunction

Yang

Xue

Kuang

et al. 2019

Korean J Physiol Pharmacol

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“…However, Ziomek et al found that tunicamycin induced a significant increase of intracellular Ca 2+ in VSMC. Still, it was independent of the activation of Ca2+ channels instead of the direct permeability of the plasma membrane, ER, and sarcoplasmic reticulum to Ca 2+ [ 31 ]. The different results may be due to other cell types.…”

Section: Introductionmentioning

confidence: 99%

Role of store-operated Ca2+ entry in cardiovascular disease

Lu¹,

Zhang²,

Su³

et al. 2022

Cell Commun Signal

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Store-operated channels (SOCs) are highly selective Ca2+ channels that mediate Ca2+ influx in non-excitable and excitable (i.e., skeletal and cardiac muscle) cells. These channels are triggered by Ca2+ depletion of the endoplasmic reticulum and sarcoplasmic reticulum, independently of inositol 1,4,5-trisphosphate (InsP3), which is involved in cell growth, differentiation, and gene transcription. When the Ca2+ store is depleted, stromal interaction molecule1 (STIM1) as Ca2+ sensor redistributes into discrete puncta near the plasma membrane and activates the protein Ca2+ release activated Ca2+ channel protein 1 (Orai1). Accumulating evidence suggests that SOC is associated with several physiological roles in endothelial dysfunction and vascular smooth muscle proliferation that contribute to the progression of cardiovascular disease. This review mainly elaborates on the contribution of SOC in the vasculature (endothelial cells and vascular smooth muscle cells). We will further retrospect the literature implicating a critical role for these proteins in cardiovascular disease. Graphical Abstract

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“…We observed that an ERS inhibitor significantly prevented VSMC contraction, whereas Tm aggravated the CAS-induced myocardial ischemia in mice, and ERS regulated CAS possibly through the MLCK/MLC pathway [101]. Ziomek et al [102] also pointed out that Tm did not activate Ca 2+ channels, but altered the Ca 2+ permeability of plasma membrane and ER, leading to an increase in [Ca 2+ ] i and initiating the VSMC contraction. Meanwhile, Tm also caused a decrease of Ca 2+ concentration in ER [99,102].…”

Section: Endoplasmic Reticulum Stressmentioning

confidence: 64%

“…Ziomek et al [102] also pointed out that Tm did not activate Ca 2+ channels, but altered the Ca 2+ permeability of plasma membrane and ER, leading to an increase in [Ca 2+ ] i and initiating the VSMC contraction. Meanwhile, Tm also caused a decrease of Ca 2+ concentration in ER [99,102]. The above studies have shed novel insights into the pathogenesis of CAS.…”

Section: Endoplasmic Reticulum Stressmentioning

confidence: 99%