Mastoparan-induced programmed cell death in the unicellular alga Chlamydomonas reinhardtii

Yordanova, Zhenya; Woltering, E.J.; Kapchina-Toteva, Veneta; Iakimova, Elena T.

doi:10.1093/aob/mcs264

Cited by 47 publications

(56 citation statements)

References 88 publications

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“…Using the cell wall‐deficient C. reinhardtii mutant strain cw15, we were, however, not able to confirm the results of Yordanova et al. (). As shown in the present communication, we observed necrotic cell death in this particular C. reinhardtii strain both after treatment with mastoparan or broad‐range cysteine and serine protease inhibitors.…”

contrasting

confidence: 93%

“…As reported by Yordanova et al. (), the mastoparan‐induced PCD in C. reinhardtii could be, at least partly, overcome by antioxidants and several broad‐range cysteine and serine protease inhibitors.…”

mentioning

confidence: 56%

“…Yordanova et al. (, ) have recently reported that the wasp venom mastoparan causes PCD in the unicellular green alga C. reinhardtii and that the mastoparan‐induced cell death can be, at least partly, prevented by addition of broad‐range cysteine or serine protease inhibitors.…”

Section: Resultsmentioning

confidence: 99%

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Protease Inhibitors Cause Necrotic Cell Death in Chlamydomonas reinhardtii by Inducing the Generation of Reactive Oxygen Species

Voigt

Woestemeyer

2015

J Eukaryotic Microbiology

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Protease inhibitors affecting the activity of the proteasome were reported to induce programmed cell death (apoptosis) in some mammalian cell lines. Proteasome activity can be suppressed by specific peptide derivatives and by N-tosyl-lysine-chloromethyl-ketone (TLCK) and N-tosyl-phenylalanine-chloromethyl-ketone (TPCK), which affect the trypsine- and chymotrypsine-like activities of the proteasome, respectively. Particularly TLCK and TPCK caused necrotic cell death in the unicellular green alga Chlamydomonas reinhardtii. As a control, the effects of these protease inhibitors on the survival of human WISH cells were also studied. Bleaching of the Chlamydomonas cells after addition of TLCK or TPCK indicated that reactive oxygen species (ROS) were involved in this process. Indeed, increased levels of ROS were detected in Chlamydomonas cells treated with TLCK or TPCK. Furthermore, cell death induced by these protease inhibitors was accelerated by illumination and prevented or slowed down by scavengers of ROS.

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confidence: 93%

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confidence: 56%

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Protease Inhibitors Cause Necrotic Cell Death in Chlamydomonas reinhardtii by Inducing the Generation of Reactive Oxygen Species

Voigt

Woestemeyer

2015

J Eukaryotic Microbiology

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“…Stimulation of PLC has been described previously (3) for rat mast cells and hepatocytes and human HL-60 leukaemia cells, whereas inhibition of PLC has been found for SH-SY5Y human neuro-blastoma cells and human astrocytoma cells (3). Results of recent studies have indicated that there is a possibility of stimulation of programmable cell death in various types of cells (4)(5)(6).…”

Section: Introductionmentioning

confidence: 92%

Effect of pertussis toxin on calcium influx in three contraction models

et al. 2014

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Abstract. Pertussis toxin (PTX) blocks G protein activation and inhibits signal transmission from the activated receptor to effectors that are specific for the G protein-coupled receptor. The aim of the present study was to evaluate the effect of PTX on vascular smooth muscle cells that were stimulated pharmacologically with phenylephrine (α-adrenoceptor agonist), mastoparan-7 (direct G-protein activator) and Bay K8644 (direct calcium channel activator). The changes in perfusion pressure that were proportional to the degree of phenylephrine-induced constriction of rat tail arteries were assessed. Concentration-response curves (CRCs) that were obtained for phenylephrine, mastoparan-7 and Bay K8644 presented a sigmoidal association. A significantly reduced calcium influx to the cytoplasm in the presence of mastoparan-7 resulted in a significant rightward shift of the CRCs with a significant reduction in maximal responses. The presence of PTX did not change mastoparan-7 and Bay K8644-induced contraction, whereas the significant inhibition of phenylephrine-induced contraction was found. The results of the experiments indicated that PTX significantly inhibited phenylephrine-induced contraction of vascular smooth muscle cells by inhibition of calcium influx from the intra-and extracellular calcium space. PTX did not change the smooth muscle contraction that was induced by mastoparan-7 and Bay K8644. The predominant effect of mastoparan-7 may be associated with other binding sites as compared to the G-protein or PTX may bind to other sites than mastoparan-7.

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“…By contrast, the inhibition of PLC by mastoparan has been demonstrated in SH-SY5Y human neuroblastoma cells and in human astrocytoma cells (1). Recent studies suggested the possibility of programmed cell death stimulation in different types of cells (2)(3)(4).…”

Section: Introductionmentioning

confidence: 99%

Direct regulation of vascular smooth muscle contraction by mastoparan-7

et al. 2013

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Abstract. Mastoparan-7 (mas-7) is a basic tetradecapeptide isolated from wasp venom, which activates guanine nucleotide-binding regulatory proteins (G-proteins) and stimulates apoptosis. In smooth muscle cells, mas-7 leads to an increase in the perfusion pressure. The main aim of this study was to evaluate the physiological effect of the direct stimulation of G-proteins in comparison to the typical stimulation of receptors in vascular smooth muscle cells (VSMCs). Experiments were performed on the isolated and perfused tail artery of Wistar rats. The contraction force in our model was measured by an increased level of perfusion pressure with a constant flow. The concentration response curves (CRCs) obtained for mas-7 were sigmoidal. In comparison to the curves for phenylephrine and vasopressin, the mas-7 curve was significantly shifted to the right with a significant reduction in maximal response. Mas-7 significantly increased the perfusion pressure for the intra-and extracellular calcium (Ca 2+ ) influx to the cytoplasm. The presence of the pertussis toxin (PT) did not affect the mas-7-induced contraction. In comparison to phenylephrine and vasopressin, all the values of perfusion pressure following stimulation of the G-proteins by mas-7 were significantly lower. The results of our experiments suggested that mas-7 significantly induces the contraction of VSMCs. The binding site for mas-7 is different from that for PT; thus, PT does not affect VSMC contraction. The tissue effect of this stimulation is comparable to the stimulatory effect of partial agonists. Current knowledge regarding the apoptosis pathway reveals the significance of Ca 2+ ions involved in this process. Therefore, mas-7 may induce apoptosis through an increase in the cytoplasmic Ca 2+ concentration; however, the use of this mechanism in anticancer therapy must be preceded by a molecule modification that eliminates the vasoconstrictive effect.

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Mastoparan-induced programmed cell death in the unicellular alga Chlamydomonas reinhardtii

Cited by 47 publications

References 88 publications

Protease Inhibitors Cause Necrotic Cell Death in Chlamydomonas reinhardtii by Inducing the Generation of Reactive Oxygen Species

Protease Inhibitors Cause Necrotic Cell Death in Chlamydomonas reinhardtii by Inducing the Generation of Reactive Oxygen Species

Effect of pertussis toxin on calcium influx in three contraction models

Direct regulation of vascular smooth muscle contraction by mastoparan-7

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