Apoptosis regulation at the mitochondria membrane level

Dadsena, Shashank; King, Louise; García‐Sáez, Ana J.

doi:10.1016/j.bbamem.2021.183716

Cited by 111 publications

(73 citation statements)

References 135 publications

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“…According to previous studies, the induction of apoptosis in osteoblasts by H 2 O 2 was due to the release of cytochrome c into the cytoplasm caused by disrupted mitochondrial membrane stability [29,50,51]. Cytochrome c promotes the activity of effector caspases in the cytoplasm to complete apoptosis [52,53]. In this study, the level of MMP reduced by H 2 O 2 treatment was maintained at control levels in FST-treated cells.…”

Section: Discussionsupporting

confidence: 63%

Protection against Oxidative Stress-Induced Apoptosis by Fermented Sea Tangle (Laminaria japonica Aresch) in Osteoblastic MC3T3-E1 Cells through Activation of Nrf2 Signaling Pathway

Kim

Cha

Hwangbo

et al. 2021

Foods

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The purpose of the present study was to explore the efficacy of fermented extract of sea tangle (Laminaria japonica Aresch, FST) with Lactobacillus brevis on DNA damage and apoptosis in hydrogen peroxide (H2O2)-stimulated osteoblastic MC3T3-E1 cells and clarify related signaling pathways. Our results showed that exposure to FST significantly improved cell viability, inhibited apoptosis, and suppressed the generation of reactive oxygen species (ROS) in H2O2-stimulated cells. In addition, H2O2 triggered DNA damage in MC3T3-E1 cells was markedly attenuated by FST pretreatment. Moreover, H2O2-induced mitochondrial dysfunctions associated with apoptotic events, including loss of mitochondrial membrane potential (MMP), decreased Bcl-2/Bcl-2 associated x-protein (Bax) ratio, and cytosolic release of cytochrome c, were reduced in the presence of FST. FST also diminished H2O2-induced activation of caspase-3, which was associated with the ability of FST to protect the degradation of poly (ADP-ribose) polymerase. Furthermore, FST notably enhanced nuclear translocation and phosphorylation of nuclear factor erythroid 2-related factor 2 (Nrf2) in the presence of H2O2 with concomitant upregulation of heme oxygenase-1 (HO-1) expression. However, artificial blockade of this pathway by the HO-1 inhibitor, zinc protoporphyrin IX, greatly abolished the protective effect of FST against H2O2-induced MC3T3-E1 cell injury. Taken together, these results demonstrate that FST could protect MC3T3-E1 cells from H2O2-induced damage by maintaining mitochondrial function while eliminating ROS along with activation of the Nrf2/HO-1 antioxidant pathway.

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Section: Discussionsupporting

confidence: 63%

Protection against Oxidative Stress-Induced Apoptosis by Fermented Sea Tangle (Laminaria japonica Aresch) in Osteoblastic MC3T3-E1 Cells through Activation of Nrf2 Signaling Pathway

Kim

Cha

Hwangbo

et al. 2021

Foods

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“…In addition, other known apoptosis inhibitors such as XIAP, HSP27 and HSP70 were also reduced ( Figure 3 e). The interactions between the different Bcl-2 protein family members determine whether mitochondrial outer membrane permeabilisation occurs and if mitochondrial factors are released in the cytoplasm [ 61 , 63 ]. Among these factors, cytochrome c stands out as a component of the apoptosome, a protein complex that engages and activates caspase 9 [ 61 , 64 ], and levels of cytochrome c were found to be increased in the SeNps-treated CT26 cells in our experiments ( Figure 3 e).…”

Section: Discussionmentioning

confidence: 99%

Anticancer Activity of Biogenic Selenium Nanoparticles: Apoptotic and Immunogenic Cell Death Markers in Colon Cancer Cells

Spyridopoulou

Aindelis

Pappa

et al. 2021

Cancers

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Colorectal cancer is a health problem with high mortality rates and prevalence. Thus, innovative treatment approaches need to be developed. Biogenic nanoparticles are nanomaterials that can be synthesised in biological systems and, compared to chemically synthesised nanoparticles, have better bioavailability while being more cost-effective, eco-friendlier, and less toxic. In our previous studies, the probiotic strain Lactobacillus casei ATCC 393 was used to synthesise selenium nanoparticles (SeNps), which were shown to inhibit colon cancer cell growth in vitro and in vivo. Herein, we have further investigated SeNps’ pro-apoptotic activity and their ability to induce immunogenic cell death (ICD) in colon cancer cells. The SeNps’ effect on Caco-2 cells growth was examined along with their potential to induce caspase activation. Moreover, the expression of typical pro-apoptotic and ICD markers were examined in SeNps-treated HT29 and CT26 cells by flow cytometry, Western blot, ELISA and fluorescence microscopy. Elevated caspase-3 activation and surface phosphatyldoserine, that subsided upon co-incubation with a pan-caspase inhibitor, were detected in SeNps-treated cells. Furthermore, nanoparticles induced modulation of the expression of various apoptosis-related proteins. We also report the detection of biomarkers involved in ICD, namely the translocation of calreticulin and ERp57, the release of HMGB1 and ATP, and the secretion of pro-inflammatory cytokines from SeNps-treated cells. Moreover, RAW246.7 macrophages exhibited a higher rate of phagocytosis against treated CT26 when compared to control cells. Taken together, our findings indicate that treatment with SeNps might be an efficient strategy to destroy tumour cells by inducing apoptotic cell death and triggering immune responses.

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“…It is well known that the induction of apoptosis in C2C12 cells by H 2 O 2 is due to the release of apoptotic proteins, such as cytochrome c, into the cytoplasm by disruption of mitochondrial membrane stability [29,41]. This is a typical process of the initiation of the intrinsic pathway among the apoptosis pathways, and is tightly regulated by members of the Bcl-2 family, which consist of anti-apoptotic and pro-apoptotic proteins [8,26]. Bcl-2 family proteins regulate the permeability of the mitochondrial outer membrane, thereby regulating the release of cytochrome c from the mitochondria to the cytoplasm [26,27].…”

Section: Discussionmentioning

confidence: 99%

“…This is a typical process of the initiation of the intrinsic pathway among the apoptosis pathways, and is tightly regulated by members of the Bcl-2 family, which consist of anti-apoptotic and pro-apoptotic proteins [8,26]. Bcl-2 family proteins regulate the permeability of the mitochondrial outer membrane, thereby regulating the release of cytochrome c from the mitochondria to the cytoplasm [26,27]. Consequently, we found that cytochrome c expression was predominantly expressed in the cytoplasm in H 2 O 2 -treated cells, but its expression was counteracted by pretreatment with AEMR, suggesting that mitochondrial integrity was maintained in the presence of AEMR.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, the expression of anti-apoptotic Bcl-2 protein was decreased by H2O2 treatment, whereas the expression of pro-apoptotic Bax protein was increased. Moreover, as the expression of the inactive form of caspase-3 was decreased by H2O2, its enzymatic activity was increased, which was correlated with the degradation of poly (ADP-ribose) polymerase (PARP), one of the substrate proteins cleaved by activated effector caspases such as caspase-3 [26,27] (Figure 5A,B). However, all these changes were blocked by AEMR pretreatment.…”

Section: Ampk Was Involved In the Protective Effect Of Aemr Against H 2 O 2 -Induced Mitochondrial Dysfunction In C2c12 Cellsmentioning

confidence: 99%

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Mori Ramulus Suppresses Hydrogen Peroxide-Induced Oxidative Damage in Murine Myoblast C2C12 Cells through Activation of AMPK

Park

Lee

et al. 2021

IJMS

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Mori Ramulus, the dried twigs of Morus alba L., has been attracting attention for its potent antioxidant activity, but its role in muscle cells has not yet been elucidated. The purpose of this study was to evaluate the protective effect of aqueous extracts of Mori Ramulus (AEMR) against oxidative stress caused by hydrogen peroxide (H2O2) in C2C12 mouse myoblasts, and in dexamethasone (DEX)-induced muscle atrophied models. Our results showed that AEMR rescued H2O2-induced cell viability loss and the collapse of the mitochondria membrane potential. AEMR was also able to activate AMP-activated protein kinase (AMPK) in H2O2-treated C2C12 cells, whereas compound C, a pharmacological inhibitor of AMPK, blocked the protective effects of AEMR. In addition, H2O2-triggered DNA damage was markedly attenuated in the presence of AEMR, which was associated with the inhibition of reactive oxygen species (ROS) generation. Further studies showed that AEMR inhibited cytochrome c release from mitochondria into the cytoplasm, and Bcl-2 suppression and Bax activation induced by H2O2. Furthermore, AEMR diminished H2O2-induced activation of caspase-3, which was associated with the ability of AEMR to block the degradation of poly (ADP-ribose) polymerase, thereby attenuating H2O2-induced apoptosis. However, compound C greatly abolished the protective effect of AEMR against H2O2-induced C2C12 cell apoptosis, including the restoration of mitochondrial dysfunction. Taken together, these results demonstrate that AEMR could protect C2C12 myoblasts from oxidative damage by maintaining mitochondrial function while eliminating ROS, at least with activation of the AMPK signaling pathway. In addition, oral administration of AEMR alleviated gastrocnemius and soleus muscle loss in DEX-induced muscle atrophied rats. Our findings support that AEMR might be a promising therapeutic candidate for treating oxidative stress-mediated myoblast injury and muscle atrophy.

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Apoptosis regulation at the mitochondria membrane level

Cited by 111 publications

References 135 publications

Protection against Oxidative Stress-Induced Apoptosis by Fermented Sea Tangle (Laminaria japonica Aresch) in Osteoblastic MC3T3-E1 Cells through Activation of Nrf2 Signaling Pathway

Protection against Oxidative Stress-Induced Apoptosis by Fermented Sea Tangle (Laminaria japonica Aresch) in Osteoblastic MC3T3-E1 Cells through Activation of Nrf2 Signaling Pathway

Anticancer Activity of Biogenic Selenium Nanoparticles: Apoptotic and Immunogenic Cell Death Markers in Colon Cancer Cells

Mori Ramulus Suppresses Hydrogen Peroxide-Induced Oxidative Damage in Murine Myoblast C2C12 Cells through Activation of AMPK

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