The ERK1/2–ATG13–FIP200 signaling cascade is required for autophagy induction to protect renal cells from hypoglycemia‐induced cell death

2021 ◽  
Author(s):  
Wenjing Guo ◽  
Qian Wang ◽  
Shihua Pan ◽  
Jinbing Li ◽  
Yuanhua Wang ◽  
...  
Keyword(s):  
Cell Death ◽  
Signaling Cascade ◽  
Renal Cells ◽  
Autophagy Induction

scholarly journals Targeting AKT/mTOR and Bcl-2 for Autophagic and Apoptosis Cell Death in Lung Cancer: Novel Activity of a Polyphenol Compound

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 534
Author(s):  
Sucharat Tungsukruthai ◽  
Onrapak Reamtong ◽  
Sittiruk Roytrakul ◽  
Suchada Sukrong ◽  
Chanida Vinayanwattikun ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Proteomic Analysis ◽  
Interaction Analysis ◽  
Time Dependent ◽  
The Novel ◽  
Protein Protein Interaction ◽  
Autophagy Induction ◽  
Acidic Vesicle

Autophagic cell death (ACD) is an alternative death mechanism in resistant malignant cancer cells. In this study, we demonstrated how polyphenol stilbene compound PE5 exhibits potent ACD-promoting activity in lung cancer cells that may offer an opportunity for novel cancer treatment. Cell death caused by PE5 was found to be concomitant with dramatic autophagy induction, as indicated by acidic vesicle staining, autophagosome, and the LC3 conversion. We further confirmed that the main death induction caused by PE5 was via ACD, since the co-treatment with an autophagy inhibitor could reverse PE5-mediated cell death. Furthermore, the defined mechanism of action and upstream regulatory signals were identified using proteomic analysis. Time-dependent proteomic analysis showed that PE5 affected 2142 and 1996 proteins after 12 and 24 h of treatment, respectively. The crosstalk network comprising 128 proteins that control apoptosis and 25 proteins involved in autophagy was identified. Protein–protein interaction analysis further indicated that the induction of ACD was via AKT/mTOR and Bcl-2 suppression. Western blot analysis confirmed that the active forms of AKT, mTOR, and Bcl-2 were decreased in PE5-treated cells. Taken together, we demonstrated the novel mechanism of PE5 in shifting autophagy toward cell death induction by targeting AKT/mTOR and Bcl-2 suppression.

Cyclooxygenase-independent inhibition of H2O2-induced cell death by S-ketoprofen in renal cells

2007 ◽  
Vol 55 (4) ◽  
pp. 295-302 ◽  
Author(s):  
Patricia Reyes-Martin ◽  
Matilde Alique ◽  
Trinidad Parra ◽  
Jaime Perez de Hornedo ◽  
Javier Lucio-Cazana
Keyword(s):  
Cell Death ◽  
Renal Cells

scholarly journals Plants expressing murine pro-apoptotic protein Bid do not have enhanced PCD

2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Anna Manara ◽  
Zahra Imanifard ◽  
Linda Fracasso ◽  
Diana Bellin ◽  
Massimo Crimi
Keyword(s):  
Cell Death ◽  
Stress Responses ◽  
Growth And Development ◽  
Active Form ◽  
Ectopic Expression ◽  
Signaling Cascade ◽  
Tobacco Plants ◽  
Truncated Protein ◽  
Apoptotic Protein ◽  
Family Protein

Abstract Objectives The purpose of this study was to explore whether plant programmed cell death (PCD) cascade can sense the presence of the animal-only BH3 protein Bid, a BCL-2 family protein known to play a regulatory role in the signaling cascade of animal apoptosis. Results We have expressed the mouse pro-apoptotic protein Bid in Arabidopsis thaliana and in Nicotiana tabacum. We did not obtain any transformed plant constitutively expressing the truncated protein (tBid—i.e. the caspase-activated form) whereas ectopic expression of the full-length protein (flBid) does not interfere with growth and development of the transformed plants. To verify whether the presence of this animal pro-apoptotic protein modified stress responses and PCD execution, both N. tabacum and A. thaliana plants constitutively expressing flBid have been studied under different stress conditions triggering cell death activation. The results show that the presence of flBid in transgenic plants did not significantly change the responses to abiotic stress (H2O2 or NO) and biotic stress treatments. Moreover, the finding that no Bid active form was present in treated tobacco plants suggests an absence of a proper activation of Bid.

scholarly journals Modulation of Glutathione Hemostasis by Inhibition of 12/15-Lipoxygenase Prevents ROS-Mediated Cell Death after Hepatic Ischemia and Reperfusion

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Moritz Drefs ◽  
Michael N. Thomas ◽  
Markus Guba ◽  
Martin K. Angele ◽  
Jens Werner ◽  
...  
Keyword(s):  
Cell Death ◽  
Western Blot ◽  
Caspase 3 ◽  
Ischemia Reperfusion ◽  
Signaling Cascade ◽  
Ischemia And Reperfusion ◽  
Hepatic Ischemia ◽  
Amino Terminal ◽  
Spectral Photometry ◽  
The Impact

Background. Reactive oxygen species- (ROS-) mediated ischemia-reperfusion injury (IRI) detrimentally impacts liver transplantation and resection. 12/15-Lipoxygenase (12/15-LOX), an antagonistic protein of the glutathione peroxidase 4 (GPX4) signaling cascade, was proven to mediate cell death in postischemic cerebral and myocardial tissue. The aim of this study was to investigate the impact of 12/15-LOX inhibition on hepatic IRI.Methods. Livers of C57BL/6 mice were exposed to 60 minutes of partial warm ischemia and 90 minutes of reperfusion after previous Baicalein administration, an inhibitor of 12/15-LOX. Tissue samples were analyzed by TUNEL assay, Western blot, and spectral photometry.Results. TUNEL labeling showed a significant reduction of hepatic cell death following baicalein pretreatment. Western Blot analysis revealed a significant downregulation of Jun-amino-terminal-kinase (JNK), caspase-3, and poly-ADP-ribose-polymerase (PARP), besides considerably lowered p44/42-MAP-kinase (ERK1/2) expression after Baicalein administration. A significant elevation of glutathione oxidation was measured in Baicalein pretreated livers.Conclusion. Our data show that inhibition of 12/15-lipoxygenase causes significant cell death reduction after hepatic ischemia and reperfusion by enhancing glutathione metabolism. We conclude that GPX4-dependent cell death signaling cascade might play a major role in development of hepatic IRI, in which the investigated proteins JNK, caspase-3, ERK1/2, and PARP might contribute to tissue damage.

scholarly journals FP018MTOR INHIBITORS PROMOTE AUTOPHAGIC NOT APOPTOTIC CELL DEATH IN PROXIMAL TUBULAR RENAL CELLS, VIA P75NTR ACTIVATION

2015 ◽  
Vol 30 (suppl_3) ◽  
pp. iii71-iii71
Author(s):  
Simona Lupinacci ◽  
Giuseppina Toteda ◽  
Donatella Vizza ◽  
Anna Perri ◽  
Paolo Gigliotti ◽  
...  
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Renal Cells ◽  
Proximal Tubular

Anti-cell death engineering of CHO cells: Co-overexpression of Bcl-2 for apoptosis inhibition, Beclin-1 for autophagy induction

2013 ◽  
Vol 110 (8) ◽  
pp. 2195-2207 ◽  
Author(s):  
Jae Seong Lee ◽  
Tae Kwang Ha ◽  
Jin Hyoung Park ◽  
Gyun Min Lee
Keyword(s):  
Cell Death ◽  
Cho Cells ◽  
Beclin 1 ◽  
Apoptosis Inhibition ◽  
Autophagy Induction

scholarly journals Autophagy: Friend or Foe in Breast Cancer Development, Progression, and Treatment

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Damian E. Berardi ◽  
Paola B. Campodónico ◽  
Maria Ines Díaz Bessone ◽  
Alejandro J. Urtreger ◽  
Laura B. Todaro
Keyword(s):  
Cell Death ◽  
Cell Survival ◽  
Anticancer Agents ◽  
Cancer Development ◽  
Nutrient Deprivation ◽  
Clinical Settings ◽  
Degradative Pathway ◽  
Autophagy Induction ◽  
Autophagy Inhibition ◽  
Catabolic Process

Autophagy is a catabolic process responsible for the degradation and recycling of long-lived proteins and organelles by lysosomes. This degradative pathway sustains cell survival during nutrient deprivation, but in some circumstances, autophagy leads to cell death. Thereby, autophagy can serve as tumor suppressor, as the reduction in autophagic capacity causes malignant transformation and spontaneous tumors. On the other hand, this process also functions as a protective cell-survival mechanism against environmental stress causing resistance to antineoplastic therapies. Although autophagy inhibition, combined with anticancer agents, could be therapeutically beneficial in some cases, autophagy induction by itself could lead to cell death in some apoptosis-resistant cancers, indicating that autophagy induction may also be used as a therapy. This paper summarizes the most important findings described in the literature about autophagy and also discusses the importance of this process in clinical settings.

ASK1-p38 MAPK/JNK signaling cascade mediates anandamide-induced PC12 cell death

2003 ◽  
Vol 85 (1) ◽  
pp. 50-61 ◽  
Author(s):  
Krishna Pada Sarker ◽  
Kamal Krishna Biswas ◽  
Munekazu Yamakuchi ◽  
Ki-Young Lee ◽  
Teruto Hahiguchi ◽  
...  
Keyword(s):  
Cell Death ◽  
P38 Mapk ◽  
Pc12 Cell ◽  
Signaling Cascade ◽  
Jnk Signaling

Necroptosis modulated by autophagy is a predominant form of melanoma cell death induced by sanguilutine

2012 ◽  
Vol 393 (7) ◽  
pp. 647-658 ◽  
Author(s):  
Jindřiška Hammerová ◽  
Stjepan Uldrijan ◽  
Eva Táborská ◽  
Alena Hyršlová Vaculová ◽  
Iva Slaninová
Keyword(s):  
Cell Death ◽  
Therapeutic Potential ◽  
Apoptotic Cell ◽  
Specific Inhibitor ◽  
Melanoma Cells ◽  
Bafilomycin A1 ◽  
Autophagy Induction ◽  
Predominant Type ◽  
Predominant Form ◽  
Lc3 Puncta

Abstract We show that the plant quaternary benzo[c]phenanthridine alkaloid sanguilutine (SL) is a strong inducer of caspase-independent non-apoptotic death in human melanoma cells. Necrostatin-1, a specific inhibitor of necroptosis, completely reversed the cytotoxic effect of SL, suggesting that necroptosis was a predominant type of cell death induced by SL in these cells. In addition, we showed that SL can trigger an autophagic response, as confirmed by GFP-LC3 puncta formation and LC3-II accumulation. Interestingly, we observed a significant decrease in the viability of melanoma cells treated with combination of autophagy inhibitors (3-methyladenine, bafilomycin-A1 and LY294002) and SL. Our results further indicated that autophagy may serve as a pro-survival mechanism, delaying the induction of necroptosis in melanoma cells. The ability of SL to induce caspase-independent non-apoptotic cell death (necroptosis) suggests its possible therapeutic potential in the treatment of apoptosis-resistant melanoma tumours. Furthermore, SL might serve as a useful tool for studying the mechanisms of necroptosis and autophagy induction and the interplay between these two processes.

scholarly journals Curcumin blocks multiple sites of the TGF-β signaling cascade in renal cells

2004 ◽  
Vol 66 (1) ◽  
pp. 112-120 ◽  
Author(s):  
Jens Gaedeke ◽  
Nancy A. Noble ◽  
Wayne A. Border
Keyword(s):  
Signaling Cascade ◽  
Renal Cells
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