6E11, a highly selective inhibitor of Receptor-Interacting Protein Kinase 1, protects cells against cold hypoxia-reoxygenation injury

Delehouzé, Claire; Leverrier-Penna, S.; Cann, Fabienne Le; Comte, Arnaud; Jacquard-Fevai, M.; Delalande, Olivier; Desban, Nathalie; Baratte, Blandine; Gallais, Isabelle; Faurez, Florence; Bonnet, Marion; Hauteville, Marcelle; Goekjian, Peter G.; Thuillier, Raphaël; Favreau, Fréderic; Vandenabeele, Peter; Hauet, Thierry; Dimanche‐Boitrel, Marie‐Thérèse; Bach, Stéphane

doi:10.1038/s41598-017-12788-4

Cited by 34 publications

(32 citation statements)

References 25 publications

(29 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In recent years, various inhibitors of necroptosis have been experimentally tested in relation to various human pathologies and used for mechanistic investigation of this process (Degterev et al 2005(Degterev et al , 2008(Degterev et al , 2013Delehouzé et al 2017;Do et al 2017;Li et al, 2018;Xie et al 2013). Among them, necrostatin-1 (Nec-1; methyl-thiohydantoin-tryptophan) was the first to be identified and since then used the most frequently (Degterev et al 2005(Degterev et al , 2008.…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective Effects of Necrostatin-1 Against Oxidative Stress–Induced Cell Damage: an Involvement of Cathepsin D Inhibition

et al. 2020

View full text Add to dashboard Cite

Necroptosis, a recently discovered form of non-apoptotic programmed cell death, can be implicated in many pathological conditions including neuronal cell death. Moreover, an inhibition of this process by necrostatin-1 (Nec-1) has been shown to be neuroprotective in in vitro and in vivo models of cerebral ischemia. However, the involvement of this type of cell death in oxidative stress-induced neuronal cell damage is less recognized. Therefore, we tested the effects of Nec-1, an inhibitor of necroptosis, in the model of hydrogen peroxide (H 2 O 2)-induced cell damage in human neuroblastoma SH-SY5Y and murine hippocampal HT-22 cell lines. The data showed that Nec-1 (10-40 μM) attenuated the cell death induced by H 2 O 2 in undifferentiated (UN-) and neuronal differentiated (RA-) SH-SY5Y cells with a higher efficacy in the former cell type. Moreover, Nec-1 partially reduced cell damage induced by 6-hydroxydopamine in UN-and RASH -SY5Y cells. The protective effect of Nec-1 was of similar magnitude as the effect of a caspase-3 inhibitor in both cell phenotypes and this effect were not potentiated after combined treatment. Furthermore, the non-specific apoptosis and necroptosis inhibitor curcumin augmented the beneficial effect of Nec-1 against H 2 O 2-evoked cell damage albeit only in RASH -SY5Y cells. Next, it was found that the mechanisms of neuroprotective effect of Nec-1 against H 2 O 2induced cell damage in SH-SY5Y cells involved the inhibition of lysosomal protease, cathepsin D, but not caspase-3 or calpain activities. In HT-22 cells, Nec-1 was protective in two models of oxidative stress (H 2 O 2 and glutamate) and that effect was blocked by a caspase inhibitor. Our data showed neuroprotective effects of the necroptosis inhibitor, Nec-1, against oxidative stress-induced cell damage and pointed to involvement of cathepsin D inhibition in the mechanism of its action. Moreover, a cell type-specific interplay between necroptosis and apoptosis has been demonstrated.

show abstract

Section: Introductionmentioning

confidence: 99%

Neuroprotective Effects of Necrostatin-1 Against Oxidative Stress–Induced Cell Damage: an Involvement of Cathepsin D Inhibition

et al. 2020

View full text Add to dashboard Cite

show abstract

“…Natural product derivative 6E11 ( 9 , RIPK1 IC 50 = 90 nmol/L) inhibited necroptosis induced by TNF- α or TRAIL, but failed to inhibit TRAIL-induced apoptosis, thus providing a novel structural type for RIPK1 inhibitors 76 .…”

Section: Inhibitors Of Necroptosismentioning

confidence: 99%

Targeting necroptosis in anticancer therapy: mechanisms and modulators

Dong

Sheng

2020

Acta Pharmaceutica Sinica B

View full text Add to dashboard Cite

Necroptosis, a genetically programmed form of necrotic cell death, serves as an important pathway in human diseases. As a critical cell-killing mechanism, necroptosis is associated with cancer progression, metastasis, and immunosurveillance. Targeting necroptosis pathway by small molecule modulators is emerging as an effective approach in cancer therapy, which has the advantage to bypass the apoptosis-resistance and maintain antitumor immunity. Therefore, a better understanding of the mechanism of necroptosis and necroptosis modulators is necessary to develop novel strategies for cancer therapy. This review will summarize recent progress of the mechanisms and detecting methods of necroptosis. In particular, the relationship between necroptosis and cancer therapy and medicinal chemistry of necroptosis modulators will be focused on.

show abstract

“…To mimic the ischemia-reperfusion found in vivo, we used a standard protocol of hypoxia-reoxygenation in human aortic endothelial cells (HAEC, Gibco, Courtaboeuf, France), cultured as recommended by the manufacturer [12]. Cells were synchronized, then treated with increasing concentrations of tannic acid, gallic acid, PGG or Phosphate Buffer Saline (PBS) during hypoxia (6 h) and reoxygenation (4 or 18 h) at 37 • C (Supplementary Figure S3).…”

Section: Effects Of Tannic Acid and Derivatives On Ros Production In mentioning

confidence: 99%

Tannic Acid Improves Renal Function Recovery after Renal Warm Ischemia–Reperfusion in a Rat Model

et al. 2020

View full text Add to dashboard Cite

Background and purpose: Ischemia–reperfusion injury is encountered in numerous processes such as cardiovascular diseases or kidney transplantation; however, the latter involves cold ischemia, different from the warm ischemia found in vascular surgery by arterial clamping. The nature and the intensity of the processes induced by ischemia types are different, hence the therapeutic strategy should be adapted. Herein, we investigated the protective role of tannic acid, a natural polyphenol in a rat model reproducing both renal warm ischemia and kidney allotransplantation. The follow-up was done after 1 week. Experimental approach: To characterize the effect of tannic acid, an in vitro model of endothelial cells subjected to hypoxia–reoxygenation was used. Key results: Tannic acid statistically improved recovery after warm ischemia but not after cold ischemia. In kidneys biopsies, 3 h after warm ischemia–reperfusion, oxidative stress development was limited by tannic acid and the production of reactive oxygen species was inhibited, potentially through Nuclear Factor erythroid-2-Related factor 2 (NRF2) activation. In vitro, tannic acid and its derivatives limited cytotoxicity and the generation of reactive oxygen species. Molecular dynamics simulations showed that tannic acid efficiently interacts with biological membranes, allowing efficient lipid oxidation inhibition. Tannic acid also promoted endothelial cell migration and proliferation during hypoxia. Conclusions: Tannic acid was able to improve renal recovery after renal warm ischemia with an antioxidant effect putatively extended by the production of its derivatives in the body and promoted cell regeneration during hypoxia. This suggests that the mechanisms induced by warm and cold ischemia are different and require specific therapeutic strategies.

show abstract

6E11, a highly selective inhibitor of Receptor-Interacting Protein Kinase 1, protects cells against cold hypoxia-reoxygenation injury

Cited by 34 publications

References 25 publications

Neuroprotective Effects of Necrostatin-1 Against Oxidative Stress–Induced Cell Damage: an Involvement of Cathepsin D Inhibition

Neuroprotective Effects of Necrostatin-1 Against Oxidative Stress–Induced Cell Damage: an Involvement of Cathepsin D Inhibition

Targeting necroptosis in anticancer therapy: mechanisms and modulators

Tannic Acid Improves Renal Function Recovery after Renal Warm Ischemia–Reperfusion in a Rat Model

Contact Info

Product

Resources

About