Apoptotic and Nonapoptotic Caspase Functions in Animal Development

Miura, Masayuki

doi:10.1101/cshperspect.a008664

Cited by 71 publications

(58 citation statements)

References 157 publications

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“…These results agree with the findings reported in previous studies where caspases have been revealed as dynamic regulatory molecules during cell differentiation (in neural cells and salivary gland in drosophila), cell morphology, stem-cell maintenance, tissue regeneration and actin-cytoskeleton reorganization (38)(39)(40)(41). On the contrary, Kouidhi et al (32) demonstrated the absence of caspase 3 at PNDs 21 and 35 in their study.…”

Section: Figsupporting

confidence: 93%

Effect of Biochanin A versus 17β estradiol in rat submandibular salivary gland

2017

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Abstract:The epigenetic nature of development mandates the observation of the effect of any exogenous substance, especially those with estrogenic activities, during critical phases of development. The submandibular gland (SMG) presents as a great model due to extensive postnatal development, and is known to be regulated and affected by hormones as well as growth factors. Herein, we observed postnatal development following low doses of Biochanin A (BCA) and 17β estradiol (E2) in rats. The pups were randomly divided into four groups: control, BCA, E2, and dimethyl sulfoxide (DMSO), and euthanized at the 6th, 15th, 30th, and 60th postnatal days (PND). SMG morphogenesis was assessed. The nuclear expression of estrogen receptor beta (ERβ) was evaluated immunohistochemically; ERβ expression was up-regulated by BCA and down-regulated by E2. Similarly, caspase three gene expression, assessed by real time polymerase chain reaction was increased in the BCA group but decreased in the E2 group. A significant decrease in epidermal growth factor gene expression was noted at PND 30. The results presented by this study provide evidence that the effect of a postnatal exposure of the SMG to Biochanin A during development could be linked to sex hormone-dependent disorders.

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Section: Figsupporting

confidence: 93%

Effect of Biochanin A versus 17β estradiol in rat submandibular salivary gland

2017

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“…Whether other cell-death proteases can be upregulated in a similar manner is a question in a long list of questions which warrant further investigation in order to decipher the underlying interconnections behind the mutual crosstalk of autophagy and apoptosis. Since caspases have been known to contribute to processes such as cellproliferation and differentiation, which are starkly contradictory to apoptosis [3], [117], [118], it is entirely possible that these misunderstood hitmen may have additional and more extensive roles in autophagy awaiting discovery. Taking all the presented findings into account, the primary conclusions of the review are that caspases can directly interact with known ATGs and consequently affect autophagy in a number of ways.…”

Section: Discussionmentioning

confidence: 99%

Caspase involvement in autophagy

2017

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Caspases are a family of cysteine proteases widely known as the principal mediators of the apoptotic cell death response, but considerably less so as the contributors to the regulation of pathways outside cellular demise. In regards to autophagy, the modulatory roles of caspases have only recently begun to be adequately described. In contrast to apoptosis, autophagy promotes cell survival by providing energy and nutrients through the lysosomal degradation of cytoplasmic constituents. Under basal conditions autophagy and apoptosis cross-regulate each other through an elaborate network of interconnections which also includes the interplay between autophagyrelated proteins (ATGs) and caspases. In this review we focus on the effects of this crosstalk at the cellular level, as we aim to concentrate the main observations from research conducted so far on the fine-tuning of autophagy by caspases. Several members of this protease-family have been found to directly interact with key ATGs involved in different tiers across the autophagic cascade. Therefore, we firstly outline the core mechanism of macroautophagy in brief. In an effort to emphasize the importance of the intricate cross-regulation of ATGs and caspases, we also present examples drawn from Drosophila and plant models regarding the contribution of autophagy to apoptotic cell death during normal development. Keywords and abbreviationsautophagy; macroautophagy; mammals; caspases; apoptosis; crosstalk; regulation AMBRA-1Activating-molecule-in-Beclin1-regulated-autophagy-1 AMPK AMP-activated-protein-kinase ATG Autophagy-related gene ATG14L ATG14-likeBcl-2 B-cell lymphoma 2 • Autophagy is implicated in many physiological and pathological processes, where apoptosis is also involved DISC Death-inducing signalling complex FADD Fas-associated protein with death domain Open Questions• Does control of autophagy by caspases represent a central or a supplementary mode of regulation of this pathway?• Is caspase activation required to control autophagy?• To what extent do caspases affect autophagy and how exactly their effects on the pathway vary across different contexts?4

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“…Caspase 3 activation has also been found to coincide with ephrin-induced EphA4 activation, albeit in an apoptotic situation (Park et al, 2013). Although Eph activation-induced apoptosis might play a role during neural development (Depaepe et al, 2005;Duffy et al, 2008), we have demonstrated previously that in EphA3-HEK293 and melanoma cells ephrinA5-induced cell contraction does not induce apoptosis (Lawrenson et al, 2002), indicating that localised caspase-3 activation and PTP-PEST cleavage in ephrin-stimulated EphA3-HEK293 cells reflects one of the non-apoptotic caspase functions that have been previously described (Miura, 2012).…”

Section: A Caspase-cleaved Ptp-pest N-terminal Ptp Fragment Controls mentioning

confidence: 99%

PTP-PEST controls EphA3 activation and ephrin-induced cytoskeletal remodelling

Mansour

Nievergall

Gegenbauer

et al. 2015

Journal of Cell Science

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Eph receptors and their corresponding membrane-bound ephrin ligands regulate cell positioning and establish tissue patterns during embryonic and oncogenic development. Emerging evidence suggests that assembly of polymeric Eph signalling clusters relies on cytoskeletal reorganisation and underlies regulation by protein tyrosine phosphatases (PTPs). PTP-PEST (also known as PTPN12) is a central regulator of actin cytoskeletal dynamics. Here, we demonstrate that an N-terminal fragment of PTP-PEST, generated through an ephrinA5-triggered and spatially confined cleavage mediated by caspase-3, attenuates EphA3 receptor activation and its internalisation. Isolation of EphA3 receptor signalling clusters within intact plasma membrane fragments obtained by detergent-free cell fractionation reveals that stimulation of cells with ephrin triggers effective recruitment of this catalytically active truncated form of PTP-PEST together with key cytoskeletal and focal adhesion proteins. Importantly, modulation of actin polymerisation using pharmacological and dominant-negative approaches affects EphA3 phosphorylation in a similar manner to overexpression of PTP-PEST. We conclude that PTP-PEST regulates EphA3 activation both by affecting cytoskeletal remodelling and through its direct action as a PTP controlling EphA3 phosphorylation, indicating its multifaceted regulation of Eph signalling.

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Apoptotic and Nonapoptotic Caspase Functions in Animal Development

Cited by 71 publications

References 157 publications

Effect of Biochanin A versus 17β estradiol in rat submandibular salivary gland

Effect of Biochanin A versus 17β estradiol in rat submandibular salivary gland

Caspase involvement in autophagy

PTP-PEST controls EphA3 activation and ephrin-induced cytoskeletal remodelling

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