Paraptosis-like cell death induced by yessotoxin

Korsnes, Mónica Suárez; Espenes, Arild; Hetland, Dyveke Lem; Hermansen, L.

doi:10.1016/j.tiv.2011.09.005

Cited by 40 publications

(32 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…PARP cleavage which is considered as a hallmark in apoptosis is absent in paraptosis [30]. Lack of PARP cleavage in paraptosis induced by yessotoxin has also been reported [14]. Similar results were also observed by [24], [35].…”

Section: Discussionsupporting

confidence: 78%

“…Involvement of MAPK in paraptosis induced by human insulin-like growth factor I receptor (IGF-IR) has been reported by [31] while [41] reported the activation of ERK1/2 and p38 protein kinases in paraptosis like cell death induce by grape seed oligomer in human glioblastoma U87 cells. [14] also showed the phosphorylation of JNK in yessotoxin induced paraptosis in BC3H1 cells. In our study we have also shown the activation of ERK1/2 protein kinase in HepG2 cells by hesperidin.…”

Section: Discussionmentioning

confidence: 88%

“…The caspase independent PCD are autophagy, mitotic catastrophe, paraptosis, exitotoxicity, Wallerian degeneration and programmed necrosis [4]. Many natural anti-cancer substances such as taxol [3], [32], yessotoxin [14], ginsenoside [20], curcumin [40], honoki [36], γ-tocotrienol [42] can induce caspase independent PCD besides the caspase dependent one. The cytotoxic effect of hesperidin triggering non apoptotic mechanisms is not well understood.…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Hesperidin Induces Paraptosis Like Cell Death in Hepatoblatoma, HepG2 Cells: Involvement of ERK1/2 MAPK

et al. 2014

View full text Add to dashboard Cite

Hesperidin, a natural flavonoid abundantly present in Citrus is known for its anti-cancer, anti-oxidant and anti-inflammatory properties. In this study we examined the effect of hesperidin on HepG2 cells. HepG2 cells treated with various concentration of hesperidin undergo a distinct type of programed cell death. Cytoplasmic vacuolization, mitochondria and endoplasmic reticulum swelling and uncondensed chromatin were observed in hesperidin treated cells. DNA electrophoresis show lack of DNA fragmentation and western blot analysis demonstrates lack of caspase activation and PARP cleavage. It was observed that hesperidin induced cell death is nonautophagic and also activate mitogen activated protein kinase ERK1/2. Taken together, the data indicate that hesperidin induces paraptosis like cell death in HepG2 cells with the activation of ERK1/2. Thus our finding suggests that hesperidin inducing paraptosis may offer an alternative tool in human liver carcinoma therapy.

show abstract

Section: Discussionsupporting

confidence: 78%

Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Hesperidin Induces Paraptosis Like Cell Death in Hepatoblatoma, HepG2 Cells: Involvement of ERK1/2 MAPK

et al. 2014

View full text Add to dashboard Cite

show abstract

“…The apoptotic pathway including caspase 3 activation was first described in the BE(2)-M17 neuroblastoma cell line [13], whereas paraptosis (BC3H1 myoblast cells) [41] and autophagy (human glioma and K-562 cells) were more recently described [15, 41, 42]. Previous work also described YTX apoptosis induction in K-562 cell line (other by activating caspase 3 and 8 (extrinsic apoptotic pathway hallmark) and decreasing anti-apoptotic Bcl-2 protein levels [15].…”

Section: Discussionmentioning

confidence: 99%

Yessotoxin, a Marine Toxin, Exhibits Anti-Allergic and Anti-Tumoural Activities Inhibiting Melanoma Tumour Growth in a Preclinical Model

et al. 2016

View full text Add to dashboard Cite

Yessotoxins (YTXs) are a group of marine toxins produced by the dinoflagellates Protoceratium reticulatum, Lingulodinium polyedrum and Gonyaulax spinifera. They may have medical interest due to their potential role as anti-allergic but also anti-cancer compounds. However, their biological activities remain poorly characterized. Here, we show that the small molecular compound YTX causes a slight but significant reduction of the ability of mast cells to degranulate. Strikingly, further examination revealed that YTX had a marked and selective cytotoxicity for the RBL-2H3 mast cell line inducing apoptosis, while primary bone marrow derived mast cells were highly resistant. In addition, YTX exhibited strong cytotoxicity against the human B-chronic lymphocytic leukaemia cell line MEC1 and the murine melanoma cell line B16F10. To analyse the potential role of YTX as an anti-cancer drug in vivo we used the well-established B16F10 melanoma preclinical mouse model. Our results demonstrate that a few local application of YTX around established tumours dramatically diminished tumour growth in the absence of any significant toxicity as determined by the absence of weight loss and haematological alterations. Our data support that YTX may have a minor role as an anti-allergic drug, but reveals an important potential for its use as an anti-cancer drug.

show abstract

“…Another type of programmed cell death, recently reported for YTX in the BC3H1 myoblast cell line, is paraptosis. 24 This kind of programmed cellular death is typical of neurons overcoat in neurodegenerative diseases as Huntington's disease and amyotrophic lateral sclerosis. 25,26 So, in this work, we study the effects of YTX over primary cortical neurons for the first time.…”

Section: −3mentioning

confidence: 99%

Translocation of PKC by Yessotoxin in an in Vitro Model of Alzheimer’s Disease with Improvement of Tau and β-Amyloid Pathology

Albrecht

Vale

Vieytes

et al. 2013

ACS Chem. Neurosci.

View full text Add to dashboard Cite

Yessotoxin is a marine phycotoxin that induces motor alterations in mice after intraperitoneal injection. In primary cortical neurons, yessotoxin treatment induced a caspase-independent cell death with an IC 50 of 4.27 nM. This neurotoxicity was enhanced by 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid and partially blocked by amiloride. Unlike previous studies, yessotoxin did not increase cyclic adenosine monophosphate levels or produce any change in phosphodiesterase 4 steady state expression in triple transgenic neurons. Since phosphodiesterases (PDEs) are engaged in learning and memory, we studied the in vitro effect of the toxin against Alzheimer's disease hallmarks and observed that pretreatment of cortical 3xTg-AD neurons with a low nanomolar concentration of yessotoxin showed a decrease expression of hyperphosphorylated tau isoforms and intracellular accumulation of amyloid-beta. These effects were accompanied with an increase in the level of the inactive isoform of the glycogen synthase kinase 3 and also by a translocation of protein kinase C from cytosol to membrane, pointing to its activation. In fact, inhibition of protein kinase C with GF109203X blocked the effect of yessotoxin over tau protein. The data presented here shows that 1 nM yessotoxin activates protein kinase C with beneficial effects over the main Alzheimer's disease hallmarks, tau and Aβ, in a cellular model obtained from 3xTg-AD fetuses. KEYWORDS: Marine toxin, yessotoxin, Alzheimer's disease, protein kinase C Y essotoxin (YTX) is a marine phycotoxin with more than 40 analogues isolated for the first time in Japanese waters. It is produced by different dinoflagellates, among them, Protoceratium reticulatum and Lingulodinium polyedrum. 1−3Originally, the toxin was included with the okadaic acid (OA) in the group of diarrheic shellfish poisoning (DSP) toxins, because they used to appear together during toxic episodes. Later, it was separated in its own group, due to different biological origin and different in vivo effects. 4 One of the main differences with OA is that YTX shows no inhibition of protein phosphatase 2A (PP2A). 5 Recently, it has been observed that, in fact, YTX and OA show an immunoregulatory effect over lymphocytes, although through protein kinase C (PKC) mediated mechanisms in the case of YTX and through PP2A mechanisms in the case of OA. 6PKC is widely expressed in neurons, and it is implicated in neuroprotection, synaptic function, and plasticity. This turns it into an important molecule in learning and memory, and its signaling disruption causes impairment in these processes. 7−9Moreover, reduced PKC levels were found in samples from patients with Alzheimer's disease (AD).10 Several pieces of evidence indicate that amyloid beta (Aβ) peptide can reduce PKC levels and also block the activation and normal function of the enzyme.11 All these findings indicate that PKC activators may constitute an interesting target for AD related pathology, as PKC isoforms are involved in memory processing and the enzyme c...

show abstract

Paraptosis-like cell death induced by yessotoxin

Cited by 40 publications

References 36 publications

Hesperidin Induces Paraptosis Like Cell Death in Hepatoblatoma, HepG2 Cells: Involvement of ERK1/2 MAPK

Hesperidin Induces Paraptosis Like Cell Death in Hepatoblatoma, HepG2 Cells: Involvement of ERK1/2 MAPK

Yessotoxin, a Marine Toxin, Exhibits Anti-Allergic and Anti-Tumoural Activities Inhibiting Melanoma Tumour Growth in a Preclinical Model

Translocation of PKC by Yessotoxin in an in Vitro Model of Alzheimer’s Disease with Improvement of Tau and β-Amyloid Pathology

Contact Info

Product

Resources

About