Transglutaminase 2 Promotes Both Caspase-dependent and Caspase-independent Apoptotic Cell Death via the Calpain/Bax Protein Signaling Pathway

Yoo, Je-Ok; Lim, Young-Cheol; Kim, Young‐Myeong; Ha, Kwon‐Soo

doi:10.1074/jbc.m111.326074

Cited by 37 publications

(34 citation statements)

References 38 publications

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“…50,51 Our results were in agreement with those from previous studies. We also observed that the translocation of Bax and cytochrome C were blocked by NAC following PDT treatment (Figure 7), which might be because ROS bursts following PDT play an important role in regulating the translocation and cytochrome C. 52 Our findings demonstrated that UCNPs-Ce6-mediated PDT induces apoptosis in THP-1 macrophages via the mitochondrial caspase pathway, which is activated by ROS bursts following PDT treatment (Figure 8). …”

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confidence: 53%

Upconversion nanoparticle-mediated photodynamic therapy induces THP-1 macrophage apoptosis via ROS bursts and activation of the mitochondrial caspase pathway

Zhu¹,

Wang²,

Zheng³

et al. 2015

IJN

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Atherosclerosis (AS) is the most vital cardiovascular disease, which poses a great threat to human health. Macrophages play an important role in the progression of AS. Photodynamic therapy (PDT) has emerged as a useful therapeutic modality not only in the treatment of cancer but also in the treatment of AS. The purpose of this study was to determine the molecular mechanisms underlying the activity of PDT, using mesoporous-silica-coated upconversion fluorescent nanoparticles encapsulating chlorin e6 (UCNPs-Ce6) in the induction of apoptosis in THP-1 macrophages. Here, we investigated the ability of UCNPs-Ce6-mediated PDT to induce THP-1 macrophage apoptosis by facilitating the induction of reactive oxygen species (ROS) and regulation of mitochondrial permeability transition pore (MPTP) to depolarize mitochondrial membrane potential (MMP). Both Bax translocation and the release of cytochrome C were examined using immunofluorescence and Western blotting. Our results indicated that the levels of ROS were significantly increased in the PDT group, resulting in both MPTP opening and MMP depolarization, which led to apoptosis. In addition, immunofluorescence and Western blotting revealed that PDT induced both Bax translocation and the release of cytochrome C, as well as upregulation of cleaved caspase-9, cleaved caspase-3, and cleaved poly(ADP-ribose) polymerase. Therefore, we demonstrated that UCNPs-Ce6-mediated PDT induces apoptosis in THP-1 macrophages via ROS bursts. The proapoptotic factor Bax subsequently translocates from the cytosol to the mitochondria, resulting in the MPTP opening and cytochrome C release. This study demonstrated the great potential of UCNPs-Ce6-mediated PDT in the treatment of AS.

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confidence: 53%

Upconversion nanoparticle-mediated photodynamic therapy induces THP-1 macrophage apoptosis via ROS bursts and activation of the mitochondrial caspase pathway

Zhu¹,

Wang²,

Zheng³

et al. 2015

IJN

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“…Anticancer drugs may induce mitochondrial dysfunction in cells via dissipation of ΔΨm leading to liberation of numerous cell death proteins from the mitochondria (24). Therefore, it was reported that the intrinsic pathway depends on the dysfunction of the mitochondria resulting from an increase in the ratio of Bak:Bcl-2 which is caused by anticancer drugs thus leading to AIF and Endo G release from the mitochondria before inducing apoptosis (25)(26)(27) which is termed caspase-independent pathways or alternatively causing cytochrome c release, activation of caspase-9 and -3 resulting in apoptosis termed the caspase-dependent pathway (28). Our results showed that DMC induced mitochondrial dysfunction (decreased levels of ΔΨm) (Fig.…”

Section: Discussionmentioning

confidence: 99%

Demethoxycurcumin induces the apoptosis of human lung cancer NCI-H460 cells through the mitochondrial-dependent pathway

Lien

Liu

et al. 2015

Oncology Reports

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Abstract. Lung cancer is the most common cause of cancerrelated mortality in the US as well as other regions of the world. Curcumin, demethoxycurcumin (DMC) and bisdemethoxycurcumin (BDMC) are the major components of Curcuma longa L. It has been reported that curcumin inhibits the growth of various types of cancer cells in vitro and in vivo. However, the mechanisms involved in the inhibition of cell growth and induced apoptosis by DMC in human lung cancer cells remain unclear. In the present study, we investigated the effect of DMC on cell death via the induction of apoptosis in NCI-H460 human lung cancer cells. Flow cytometric assay was used to examine the total percentage of viable cells, the population of cells in the sub-G1 phase of the cell cycle, the level of reactive oxygen species (ROS), Ca 2+ production, mitochondrial membrane potential (ΔΨm) and caspase activity. Western blotting was used to examine the changes in the expression of cell cycle-and apoptosis-associated proteins. Confocal microscopy was used to examine the translocation of apoptosis-associated proteins. The results indicated that DMC significantly induced cell morphological changes and decreased the percentage of viable NCI-H460 cells and DMC induced apoptosis based on the cell distribution in the sub-G1 phase. Moreover, DMC promoted ROS and Ca 2+ production and decreased the level of ΔΨm and promoted the activities of caspase-3, -8 and -9. The Western blotting results showed that DMC promoted the expression of AIF, Endo G and PARP. The levels of Fas ligand (Fas L) and Fas were also upregulated. Furthermore, DMC promoted expression of ER stress-associated proteins such as GRP78, GADD153, IRE1β, ATF-6α, ATF-6β and caspase-4. Based on the findings, we suggest that DMC may be used as a novel anticancer agent for the treatment of lung cancer in the future.

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“…It should be interesting that cystamine attenuated not only TG2 activity but also TG2 expression, which were induced by OGD. Although cystamine is a transglutaminase inhibitor and its underlying mechanism remains unknown, previous reports also demonstrated the suppression of TG2 expression by cystamine (31,32). Then by using TG2-specific inhibitor R283 and TG2-specific siRNA, we attempted to confirm whether or not TG2 is involved in suppression of PAC1 in OGD-induced ER stress.…”

Section: Discussionmentioning

confidence: 96%

Pituitary Adenylate Cyclase-activating Polypeptide Type 1 Receptor (PAC1) Gene Is Suppressed by Transglutaminase 2 Activation

Miura

Kambe

Inoue

et al. 2013

Journal of Biological Chemistry

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Background:The expression of PAC1, a specific receptor for PACAP, is decreased in brain ischemia. Results: PAC1 expression was attenuated by inactivation of Sp1 through cross-linking by transglutaminase 2 (TG2) activated by ER stress. Conclusion: TG2 is involved in negative regulation of PAC1 gene expression. Significance: Suppression of PAC1 by TG2 might be involved in neuronal damage from brain ischemia.

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Transglutaminase 2 Promotes Both Caspase-dependent and Caspase-independent Apoptotic Cell Death via the Calpain/Bax Protein Signaling Pathway

Cited by 37 publications

References 38 publications

Upconversion nanoparticle-mediated photodynamic therapy induces THP-1 macrophage apoptosis via ROS bursts and activation of the mitochondrial caspase pathway

Upconversion nanoparticle-mediated photodynamic therapy induces THP-1 macrophage apoptosis via ROS bursts and activation of the mitochondrial caspase pathway

Demethoxycurcumin induces the apoptosis of human lung cancer NCI-H460 cells through the mitochondrial-dependent pathway

Pituitary Adenylate Cyclase-activating Polypeptide Type 1 Receptor (PAC1) Gene Is Suppressed by Transglutaminase 2 Activation

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