Programmed cell death 50 (and beyond)

Lockshin, Richard A.

doi:10.1038/cdd.2015.126

Cited by 43 publications

(33 citation statements)

References 73 publications

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“…In normal cells, the onset of moderate autophagy usually inhibits the occurrence of apoptosis [39]. However, excessive autophagy in cells stimulated by drugs and other factors may play an important role in apoptosis [40, 41]. In the present study, we found that both apoptosis and autophagy were induced after isogambogenic acid treatment.…”

Section: Discussionsupporting

confidence: 59%

Isogambogenic Acid Inhibits the Growth of Glioma Through Activation of the AMPK-mTOR Pathway

Zhao

Peng

Shu

et al. 2017

Cell Physiol Biochem

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Background/Aims: Glioma is the most devastating cancer in the brain and has a poor prognosis in adults. Therefore, there is a critical need for novel therapeutic strategies for the management of glioma patients. Isogambogenic acid, an active compound extracted from the Chinese herb Garcinia hanburyi, induces autophagic cell death. Methods: Cell viability was detected with MTT assays. Cell proliferation was assessed using the colony formation assay. Morphological changes associated with autophagy and apoptosis were tested by TEM and Hoechst staining, respectively. The apoptosis rate was measured by flow cytometry. Western blot, immunofluorescence and immunohistochemical analyses were used to detect protein expression. U87-derived xenografts were established for the examination of the effect of isogambogenic acid on glioma growth in vivo. Results: Isogambogenic acid induced autophagic death in U87 and U251 cells, and blocking late-stage autophagy markedly enhanced the antiproliferative activities of isogambogenic acid. Moreover, we observed the activation of AMPK-mTOR signalling in isogambogenic acid-treated glioma cells. Furthermore, the activation of AMPK or the inhibition of mTOR augmented isogambogenic acid-induced autophagy. Inhibition of autophagy attenuated apoptosis in isogambogenic acid-treated glioma cells. Finally, isogambogenic acid inhibited the growth of U87 glioma in vivo. Conclusion: Isogambogenic acid inhibits the growth of glioma via activation of the AMPK-mTOR signalling pathway, which may provide evidence for future clinical applications in glioma therapy.

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Section: Discussionsupporting

confidence: 59%

Isogambogenic Acid Inhibits the Growth of Glioma Through Activation of the AMPK-mTOR Pathway

Zhao

Peng

Shu

et al. 2017

Cell Physiol Biochem

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“…Various cell death events have been described at the cellular level dating as far back as the late 19th century [reviewed in ]. The knowledge that cell death is a regulated process did not emerge until the latter half of the 20th century, and it was not until the beginning of the 21st century that the existence and physiological relevance of non‐apoptotic cell death was formally recognized . Within this context, it seems likely that our understanding of ferroptosis and other forms of cell sabotage is incomplete and that further evidence could be adduced that these processes represent adaptive features of biological systems.…”

Section: Discussionmentioning

confidence: 99%

Ferroptosis: bug or feature?

Dixon

2017

Immunological Reviews

251

187

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Ferroptosis is an iron-dependent, oxidative form of non-apoptotic cell death. This form of cell death does not share morphological, biochemical, or genetic similarities with classic necrosis, necroptosis, parthanatos, or other forms of non-apoptotic cell death. Ferroptosis can be triggered by depleting the cell of the amino acid cysteine, or by inhibiting the phospholipid hydroperoxidase glutathione peroxidase 4 (GPX4). Why certain stimuli trigger ferroptosis instead of another form of cell death, and whether this process could be adaptive in vivo, are two major unanswered questions concerning this process. Emerging evidence and consideration of related non-apoptotic pathways suggest that ferroptosis could be an adaptive process, albeit one regulated and executed in a manner very different from apoptosis and other forms of cell death.

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“…The proportion of proteasome immune subunits influences the activation of macrophages and their polarization into either an ED1- or ED2-phenotype [ 45 ]. Therefore, the change in LMP2 and LMP7 subunit levels in cell subpopulations can be associated with the activation of macrophages type 2.…”

Section: Resultsmentioning

confidence: 99%

Change in the Content of Immunoproteasomes and Macrophages in Rat Liver At the Induction of DonorSpecific Tolerance

et al. 2017

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Induction of donor specific tolerance (DST) by the introduction of donor cells into a recipient’s portal vein is one of the approaches used to solve the problem of transplant engraftment. However, the mechanism of DST development remains unclear to this moment. In the present work, we first studied the change in the content of immunoproteasomes and macrophages of the liver at early stages of the development of allospecific portal tolerance in rats by Western blotting and flow cytofluorimetry. On the basis of the data obtained, we can conclude that the induction of DST is an active process characterized by two phases during which the level of the proteasome immune subunits LMP2 and LMP7 in liver mononuclear cells, including Kupffer cells, and the number of Kupffer cells change. The first phase lasts up to 5 days after the beginning of DST induction; the second phase – from 5 to 14 days. In both phases, the level of the subunits LMP2 and LMP7 in the total pool of mononuclear cells and Kupffer cells increases, with maximum values on days 1 and 7. In addition, the total number of Kupffer cells increases in both phases with a shift in several days. The most noticeable changes take place in the second phase. The third day is characterized by a lower content of mononuclear cells expressing immunoproteasomes compared to the control value in native animals. Presumably, at this time point a “window of opportunity” appears for subsequent filling of an empty niche with cells of different subpopulations and, depending on this fact, the development of tolerance or rejection. The results obtained raise the new tasks of finding ways to influence the cellular composition in the liver and the expression of immunoproteasomes on the third day after the beginning of DST induction to block the development of rejection.

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Programmed cell death 50 (and beyond)

Cited by 43 publications

References 73 publications

Isogambogenic Acid Inhibits the Growth of Glioma Through Activation of the AMPK-mTOR Pathway

Isogambogenic Acid Inhibits the Growth of Glioma Through Activation of the AMPK-mTOR Pathway

Ferroptosis: bug or feature?

Change in the Content of Immunoproteasomes and Macrophages in Rat Liver At the Induction of DonorSpecific Tolerance

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