Suppression effects of O-demethyldemethoxycurcumin on thapsigargin triggered on endoplasmic reticulum stress in SK-N-SH cells

Janyou, Adchara; Changtam, Chatchawan; Suksamrarn, Apichart; Tocharus, Chainarong; Tocharus, Jiraporn

doi:10.1016/j.neuro.2015.08.005

Cited by 15 publications

(13 citation statements)

References 40 publications

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“…TG has been implicated as a potent inductor of ER stress and apoptotic cell death [ 24 , 25 ]. To determine whether SOCCs contribute TG- induced reduction of cell viability, an MTT assay was performed in TG-treated astrocytes after 5 and 24 h. At the earlier time point, TG had no effect on cell viability despite the significant increase in both TNF-α and IL-6 production.…”

Section: Resultsmentioning

confidence: 99%

STIMs and Orai1 regulate cytokine production in spinal astrocytes

Gao

Xia

Muñoz

et al. 2016

J Neuroinflammation

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BackgroundOur previous study demonstrated that a store-operated calcium channel (SOCC) inhibitor (YM-58483) has central analgesic effects. However, the cellular and molecular mechanisms of such effects remain to be determined. It is well-known that glial cells play important roles in central sensitization. SOC entry (SOCE) has been implicated in many cell types including cortical astrocytes. However, the role of the SOCC family in the function of astrocytes has not been determined. Here, we thoroughly investigated the expression and the functional significance of SOCCs in spinal astrocytes.MethodsPrimary cultured astrocytes were prepared from neonatal (P2–P3) CD1 mice. Expressions of mRNAs and proteins were respectively assessed by real-time PCR and Western blot analysis. SOCE was measured using a calcium imaging system. Live-cell STIM1 translocation was detected using a confocal microscope. Cytokine levels were measured by the enzyme-linked immunosorbent assay.ResultsWe found that the SOCC family is expressed in spinal astrocytes and that depletion of calcium stores from the endoplasmic reticulum by cyclopiazonic acid (CPA) resulted in a large sustained calcium entry, which was blocked by SOCC inhibitors. Using the siRNA knockdown approach, we identified STIM1 and Orai1 as primary components of SOCCs in spinal astrocytes. We also observed thapsigargin (TG)- or CPA-induced puncta formation of STIM1 and Orai1. In addition, activation of SOCCs remarkably promoted TNF-α and IL-6 production in spinal astrocytes, which were greatly attenuated by knockdown of STIM1 or Orai1. Importantly, knockdown of STIM2 and Orai1 dramatically decreased lipopolysaccharide-induced TNF-α and IL-6 production without changing cell viability.ConclusionsThis study presents the first evidence that STIM1, STIM2, and Orai1 mediate SOCE and are involved in cytokine production in spinal astrocytes. Our findings provide the basis for future assessment of SOCCs in pain and other central nervous system disorders associated with abnormal astrocyte activities.

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Section: Resultsmentioning

confidence: 99%

STIMs and Orai1 regulate cytokine production in spinal astrocytes

Gao

Xia

Muñoz

et al. 2016

J Neuroinflammation

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“…As ER stress and the UPR pathway are highly likely involved in propofol toxicity, efforts on identifying potential therapeutic candidates that reverse such process could be helpful to maintain cellular homeostasis under high concentrations of propofol. For example, O-demethyldemethoxycurcumin, a curcumin analogue, has been shown to downregulate the expression of several ER stress signaling molecules, including PERK, IRE-1, and CHOP, and has neuroprotective effect against ER stress-induced cell death [ 37 ]. Among the downregulated genes, NDUFA3, NDUF2, ATP5I, ATP5J2, ATP5G1, and COX7B are related to mitochondrial oxidative phosphorylation.…”

Section: Discussionmentioning

confidence: 99%

Effects of Propofol Treatment in Neural Progenitors Derived from Human-Induced Pluripotent Stem Cells

Long

Han

et al. 2017

Neural Plasticity

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Propofol is an intravenous anesthetic that has been widely used in clinics. Besides its anesthetic effects, propofol has also been reported to influence the regulation of the autonomic system. Controversies exist with regard to whether propofol exposure is safe for pregnant women and young children. In this work, human-induced pluripotent stem cell- (hiPSC-) derived neural progenitor cells (NPCs) were treated with propofol at 20, 50, 100, or 300 μM for 6 h or 24 h, and acute and subacute cell injury, cell proliferation, and apoptosis were evaluated. Comparison of genome-wide gene expression profiles was performed for treated and control iPSC-NPCs. Propofol treatment for 6 h at the clinically relevant concentration (20 or 50 μM) did not affect cell viability, apoptosis, or proliferation, while propofol at higher concentration (100 or 300 μM) decreased NPC viability and induced apoptosis. In addition, 20 μM propofol treatment for 6 h did not alter global gene expression. In summary, propofol treatment at commonly practiced clinical doses for 6 h did not have adverse effects on hiPSC-derived NPCs. In contrast, longer exposure and/or higher concentration could decrease NPC viability and induce apoptosis.

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Section: Introductionmentioning

confidence: 99%

“…1) induces endoplasmic reticulum stress, and may induce multiple cells to undergo endoplasmic reticulum stress and apoptosis (14). It has been demonstrated that thapsigargin may inhibit A549 cell growth, the source of which type II alveolar epithelial cells, and induce apoptosis (14). Concurrently, thapsigargin Thapsigargin induces apoptosis of prostate cancer through cofilin-1 and paxillin may induce leukemic K562 cells to undergo apoptosis in response to endoplasmic reticulum stress (15).…”

Section: Introductionmentioning

confidence: 99%

Thapsigargin induces apoptosis of prostate cancer through cofilin‑1 and paxillin

Huang

Wang

2018

Oncol Lett

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Abstract. It is widely considered that endoplasmic reticulum stress may rapidly induce apoptosis. The aim of the present study was to investigate the effect of thapsigargin on the induction of apoptosis in prostate cancer cells, and to explore its possible mechanism. A Cell Counting Kit-8 was selected to determine the effect of thapsigargin (0, 1, 10 and 100 nM) on the proliferation of PC3 cells. Cell proliferation of the prostate cancer cells was effectively inhibited by treatment with thapsigargin, and thapsigargin significantly increased the rate of apoptosis and caspase-3/9 activities in prostate cancer cells. The protein expression of phosphorylated (p)-RAC-α serine threonine-protein kinase, p-mechanistic target of rapamycin, F-actin and paxillin were significantly decreased, and cofilin-1 protein expression was significantly increased by treatment with thapsigargin in prostate cancer cells. Overall, the data of the present study revealed that thapsigargin induced apoptosis in prostate cancer cells through cofilin-1 and paxillin.

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Suppression effects of O-demethyldemethoxycurcumin on thapsigargin triggered on endoplasmic reticulum stress in SK-N-SH cells

Cited by 15 publications

References 40 publications

STIMs and Orai1 regulate cytokine production in spinal astrocytes

STIMs and Orai1 regulate cytokine production in spinal astrocytes

Effects of Propofol Treatment in Neural Progenitors Derived from Human-Induced Pluripotent Stem Cells

Thapsigargin induces apoptosis of prostate cancer through cofilin‑1 and paxillin

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