β-actin is required for mitochondria clustering and ROS generation in TNF-induced, caspase-independent cell death

Li, Jinquan; Li, Qinxi; Xie, Changchuan; Zhou, Hongyu; Wang, Yuqian; Zhang, Na; Shao, Hanjuan; Chan, Siu Chiu; Peng, Xuan‐xian; Lin, Sheng; Han, Jiahuai

doi:10.1242/jcs.01339

Cited by 58 publications

(48 citation statements)

References 55 publications

(92 reference statements)

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“…The aggregation of mitochondria in the perinuclear region of postmitotic cells can have different reasons. Perinuclear clustering of mitochondria has been observed in apoptosis as well as in necrosis (Thomas et al, 2000;Li et al, 2004) but we did not observe any caspase-3 activation in adherent postmitotic cells (data not shown), indicating that cells were not undergoing apoptosis. Overexpression of fusion proteins Mfn1 and Mfn2 in Hela cells also resulted in clustering of interconnected mitochondria (Eura et al, 2003).…”

Section: Discussionmentioning

confidence: 57%

Morpho-dynamic changes of mitochondria during ageing of human endothelial cells

Jendrach

Pohl

Vöth

et al. 2005

Mechanisms of Ageing and Development

141

105

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Mitochondrial morphology is regulated in many cultured eukaryotic cells by fusion and fission of mitochondria. A tightly controlled balance between fission and fusion events is required to ensure normal mitochondrial and cellular functions. During ageing, mitochondria are undergoing significant changes on the functional and morphological level. The effect of ageing on fusion and fission of mitochondria and consequences of altered fission and fusion activity are still unknown although theoretical models on ageing consider the significance of these processes. Human umbilical vein endothelial cells (HUVECs) have been established as a cell culture model to follow mitochondrial activity and dysfunction during the ageing process. Mitochondria of old and postmitotic HUVECs showed distinct alterations in overall morphology and fine structure, and furthermore, loss of mitochondrial membrane potential. In parallel, a decrease of intact mitochondrial DNA (mtDNA) was observed. Fission and fusion activity of mitochondria were quantified in living cells. Mitochondria of old HUVECs showed a significant and equal decrease of both fusion and fission activity indicating that these processes are sensitive to ageing and could contribute to the accumulation of damaged mitochondria during ageing. #

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Section: Discussionmentioning

confidence: 57%

Morpho-dynamic changes of mitochondria during ageing of human endothelial cells

Jendrach

Pohl

Vöth

et al. 2005

Mechanisms of Ageing and Development

141

105

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“…However, previous studies suggest the existence of mitochondria or/ and caspases-independent cell death in programmed cell death (PCD). For instance, it has been variously reported that apoptotic pathway was activated by stimuli in a mitochondria-dependent and -independent (MacDonald et al, 1999) or caspase-independent (Kang et al, 2004;Li et al, 2004;Shrivastava et al, 2006;Zhang et al, 2011) or both mitochondria-and caspase-independent manner (Chauhan et al, 2004;Bhalla et al, 2009). Our results showed that Dic did not induced any mitochondrial depolarization and caspase-3 inhibition did not prevent Dic-induced A549 cell death indicating that Dic induced a mitochondria-and caspase-3-independent A549 cell apoptosis (Figure 4).…”

Section: Discussionmentioning

confidence: 99%

Dihydroartemisinine Enhances Dictamnine-induced Apoptosis via a Caspase Dependent Pathway in Human Lung Adenocarcinoma A549 Cells

An¹,

Liu²,

Zhang³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Dictamnine (Dic) has the ability to exert cytotoxicity in human cervix, colon, and oral carcinoma cells and dihydroartemisinin (DHA) also has potent anticancer activity on various tumour cell lines. This report explores the molecular mechanisms by which Dic treatment and combination treatment with DHA and Dic cause apoptosis in human lung adenocarcinoma A549 cells. Dic treatment induced concentration-and time-dependent cell death. FCM analysis showed that Dic induced S phase cell cycle arrest at low concentration and cell apoptosis at high concentration in which loss of mitochondrial membrane potential (ΔΨm) was not involved. In addition, inhibition of caspase-3 using the specific inhibitor, z-DQMD-fmk, did not attenuate Dic-induced apoptosis, implying that Dic-induced caspase-3-independent apoptosis. Combination treatment with DHA and Dic dramatically increased the apoptotic cell death compared to Dic alone. Interestingly, pretreatment with z-DQMD-fmk significantly attenuated DHA and Dic co-induced apoptosis, implying that caspase-3 plays an important role in Dic and DHA co-induced cell apoptosis. Collectively, we found that Dic induced S phase cell cycle arrest at low concentration and cell apoptosis at high concentration in which mitochondria and caspase were not involved and DHA enhanced Dic induced A549 cell apoptosis via a caspase-dependent pathway.

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“…In our attempts to determine such a molecule, we blocked IFN-␥, IFN␣, FasL, and TRAIL; however, the neutralization of these molecules alone or in combination did not rescue NB cells from the AS-induced "delayed" death (data not shown). TNF-␣ can trigger caspase-dependent and caspase-independent cell death; the latter can be mediated by cathepsin B or reactive oxygen species in tumors of different origin (24,26,36,37). Currently available cathepsin B inhibitors, including CA074Me, did not prevent the "delayed" death in NBs.…”

Section: Discussionmentioning

confidence: 99%

Cytotoxic T Lymphocytes Induce Caspase-Dependent and -Independent Cell Death in Neuroblastomas in a MHC-Nonrestricted Fashion

Geer¹,

Kiessling²,

Levitsky

et al. 2006

The Journal of Immunology

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The MHC class I- restricted processing and presentation pathway is frequently nonfunctional in tumor cells; therefore, the direct targeting of tumor cells by CTLs may be difficult, if at all possible, to achieve. We used neuroblastoma (NB), which represents a striking example of a tumor with an impaired MHC class I pathway, as a model to study bystander effects of activated T lymphocytes on tumor cells. We found that NB cell lines are susceptible to killing by differentiated CD8+ CTL clones in a MHC class I-nonrestricted manner that involves two programs of cell death distinguished on the basis of different kinetics, sensitivities to caspase inhibitors, and cytokine-blocking reagents. The “early” death exhibited characteristic features of apoptosis, whereas the “delayed” caspase-independent death exhibited features associated with necrosis and was partially inhibited by TNF-α-blocking and prevented by overexpression of Bcl-2 or Bcl-xL. Our data reveal a previously unappreciated complexity of death pathways induced in tumor cells by immune activation and suggest that redirecting nonspecific effector CTLs to even a small proportion of NB cells or activating CTLs in a tumor’s proximity may have therapeutic effects in patients with NB.

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β-actin is required for mitochondria clustering and ROS generation in TNF-induced, caspase-independent cell death

Cited by 58 publications

References 55 publications

Morpho-dynamic changes of mitochondria during ageing of human endothelial cells

Morpho-dynamic changes of mitochondria during ageing of human endothelial cells

Dihydroartemisinine Enhances Dictamnine-induced Apoptosis via a Caspase Dependent Pathway in Human Lung Adenocarcinoma A549 Cells

Cytotoxic T Lymphocytes Induce Caspase-Dependent and -Independent Cell Death in Neuroblastomas in a MHC-Nonrestricted Fashion

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