Autophagy as a defense strategy against stress: focus on Paracentrotus lividus sea urchin embryos exposed to cadmium

Chiarelli, Roberto; Martino, Chiara; Agnello, Maria; Bosco, Liana; Roccheri, Maria Carmela

doi:10.1007/s12192-015-0639-3

Cited by 55 publications

(34 citation statements)

References 65 publications

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“…However, Kobayashi et al (50) reported that suppression of autophagy exerted protective effects against HG-mediated cardiomyocyte injury. In the present study, the results also indicated that the HG group displayed increased apoptosis compared with the NG group, and promotion of autophagy promotes apoptosis, which is a stress phenomenon (51).…”

Section: Discussionsupporting

confidence: 68%

Lycopene attenuates high glucose‑mediated apoptosis in MPC5 podocytes by promoting autophagy via the PI3K/AKT signaling pathway

Wang

Zhi

et al. 2020

Exp Ther Med

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Podocyte injury serves an important role during the progression of diabetic nephropathy (DN), and lycopene (Lyc) may display a potential protective effect against DN progression. The effects of Lyc on high glucose (HG)-induced podocyte apoptosis and the underlying mechanisms are not completely understood; therefore, the present study aimed to investigate the effects of Lyc on HG-induced MPC5 podocyte apoptosis and the underlying mechanism. In the present study, MPC5 podocytes were exposed to HG and different doses of Lyc. MPC5 podocyte viability and apoptosis were assessed by performing the MTT assay and flow cytometry, respectively. To explore the effects of Lyc on the PI3K/AKT signaling pathway and autophagy, LY294002 (LY) and 3-methyladenine (3-MA) were used as PI3K and autophagy inhibitors, respectively. The expression levels of nephrin, podocin, apoptosis-related proteins (Bax, Bcl-2 and cleaved caspase-3), autophagy-related proteins [Beclin-1 and microtubule associated protein 1 light chain 3 (LC3)II/LC3I] and certain key proteins involved in the PI3K/AKT signaling pathway were measured via western blotting. The results suggested that Lyc reversed the inhibitory effect of HG on cell viability, and the protein expression levels of nephrin and podocin, as well as the promoting effect of HG on MPC5 podocyte apoptosis. In addition, under HG conditions, Lyc upregulated the phosphorylation levels of PI3K and AKT, and reduced HG-and LY-mediated MPC5 podocyte apoptosis. Moreover, Lyc further increased HG-induced protein expression levels of Beclin-1 and LC3II/LC3I, and attenuated LY-mediated inhibition of HG-induced MPC5 podocyte autophagy. In addition, the effects of Lyc on HG-mediated MPC5 podocyte apoptosis were alleviated by 3-MA. Therefore, the present study suggested that Lyc may protect against HG-induced MPC5 podocyte apoptosis by promoting autophagy activity via activation of the PI3K/AKT signaling pathway.

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Section: Discussionsupporting

confidence: 68%

Lycopene attenuates high glucose‑mediated apoptosis in MPC5 podocytes by promoting autophagy via the PI3K/AKT signaling pathway

Wang

Zhi

et al. 2020

Exp Ther Med

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“…In fact, these two processes are more often than not mutually exclusive [10][11][12], and often activation of one pathway over another can mean the difference between an adaptive or death response [12,78,88]. Our results demonstrated a clear activation of apoptosis over autophagy in our susceptible coral species, probably triggered by excessive immune stress [12,78]. The induction of apoptosis over autophagy is possibly a result of the inability of susceptible corals to respond to the stressor and/or limited plasticity in their response.…”

Section: (B) Autophagy Is Key In Disease-tolerant Coral Speciesmentioning

confidence: 61%

“…Corals that recover post-temperature stress and bleaching are characterized by inhibition of apoptotic pathways, while those that experience mortality following these events are marked by increased apoptotic activity [77]. In other invertebrates, apoptosis is the last resort under stressful conditions, and if stress continues, death results due to excessive cell death [78].…”

Section: (A) Apoptosis Is Activated In Disease-susceptible Speciesmentioning

confidence: 99%

Life or death: disease-tolerant coral species activate autophagy following immune challenge

Fuess

Weil

et al. 2017

Proc. R. Soc. B.

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Global climate change has increased the number and severity of stressors affecting species, yet not all species respond equally to these stressors. Organisms may employ cellular mechanisms such as apoptosis and autophagy in responding to stressful events. These two pathways are often mutually exclusive, dictating whether a cell adapts or dies. In order to examine differences in cellular response to stress, we compared the immune response of four coral species with a range of disease susceptibility. Using RNA-seq and novel pathway analysis, we were able to identify differences in response to immune stimulation between these species. Disease-susceptible species activated pathways associated with apoptosis. By contrast, disease-tolerant species and activated autophagic pathways. Moderately susceptible species activated a mixture of these pathways. These findings were corroborated by apoptotic caspase protein assays, which indicated increased caspase activity following immune stimulation in susceptible species. Our results indicate that in response to immune stress, disease-tolerant species activate cellular adaptive mechanisms such as autophagy, while susceptible species turn on cell death pathways. Differences in these cellular maintenance pathways may therefore influence the organismal stress response. Further study of these pathways will increase understanding of differential stress response and species survival in the face of changing environments.

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“…Autophagy contributes to maintenance of cellular homeostasis. It regulates elimination and recycling of damaged intracellular compartments, also providing energy (ATP) for the apoptotic machinery [ 52 ]. Thus, human cells and embryos can tolerate chemical injury (e.g., heptadienal), trying to reduce its harmful effects and damages.…”

Section: Discussionmentioning

confidence: 99%

Diatom-Derived Polyunsaturated Aldehydes Activate Similar Cell Death Genes in Two Different Systems: Sea Urchin Embryos and Human Cells

Galasso

Celentano

Costantini

et al. 2020

IJMS

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Programmed cell death, such as apoptosis and autophagy, are key processes that are activated early on during development, leading to remodelling in embryos and homeostasis in adult organisms. Genomic conservation of death factors has been largely investigated in the animal and plant kingdoms. In this study, we analysed, for the first time, the expression profile of 11 genes involved in apoptosis (extrinsic and intrinsic pathways) and autophagy in sea urchin Paracentrotus lividus embryos exposed to antiproliferative polyunsaturated aldehydes (PUAs), and we compared these results with those obtained on the human cell line A549 treated with the same molecules. We found that sea urchins and human cells activated, at the gene level, a similar cell death response to these compounds. Despite the evolutionary distance between sea urchins and humans, we observed that the activation of apoptotic and autophagic genes in response to cytotoxic compounds is a conserved process. These results give first insight on death mechanisms of P. lividus death mechanisms, also providing additional information for the use of this marine organism as a useful in vitro model for the study of cell death signalling pathways activated in response to chemical compounds.

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Autophagy as a defense strategy against stress: focus on Paracentrotus lividus sea urchin embryos exposed to cadmium

Cited by 55 publications

References 65 publications

Lycopene attenuates high glucose‑mediated apoptosis in MPC5 podocytes by promoting autophagy via the PI3K/AKT signaling pathway

Lycopene attenuates high glucose‑mediated apoptosis in MPC5 podocytes by promoting autophagy via the PI3K/AKT signaling pathway

Life or death: disease-tolerant coral species activate autophagy following immune challenge

Diatom-Derived Polyunsaturated Aldehydes Activate Similar Cell Death Genes in Two Different Systems: Sea Urchin Embryos and Human Cells

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