Nonapoptotic functions of caspases: caspases as regulatory molecules for immunity and cell-fate determination

Kuranaga, Erina; Miura, Masayuki

doi:10.1016/j.tcb.2007.01.001

Cited by 167 publications

(155 citation statements)

References 80 publications

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“…It is therefore possible that reduced caspase-3 activity by maternal NR may contribute to the reduced ureteric branching and nephrogenesis. While apoptotic process may be necessary for development, recent evidence suggests that caspases mediate various cell processes such as motility, differentiation, and proliferation (36). Further study is underway to investigate the role of caspase-3 in renal development.…”

Section: Articlesmentioning

confidence: 99%

Maternal nutrient restriction inhibits ureteric bud branching but does not affect the duration of nephrogenesis in rats

Awazu

Hida

2015

Pediatr Res

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Background: Maternal nutrient restriction produces offspring with fewer nephrons. We studied whether the reduced nephron number is due to the inhibition of ureteric branching or early cessation of nephrogenesis in rats. Signaling pathways involved in kidney development were also examined. Methods: The offspring of dams given food ad libitum (control (CON)) and those subjected to 50% food restriction (nutrient restriceted (NR)) were examined. results: At embryonic day 13 (E13), there was no difference between NR and CON in body weight or kidney size. Ureteric buds branched once in both NR and CON. At E14 and E15, body and kidney size were significantly reduced in NR. Ureteric bud tip numbers were also reduced to 50% of CON. On the other hand, the disappearance of nephrogenic zone and a nephron progenitor marker Cited1 was not different between CON and NR. The final glomerular number of NR was 80% of CON. Activated extracellular signal-regulated kinase (ERK), p38, PI3K, Akt, and mammallian target of rapamycin (mTOR), and protein expression of β-catenin were downregulated at E15. conclusion: Ureteric branching is inhibited and developmentally regulated signaling pathways are downregulated at an early stage by maternal nutrient restriction. These changes, not early cessation of nephrogenesis, may be a mechanism for the inhibited kidney growth and nephrogenesis. t he concept that disturbed intrauterine organogenesis affects the health and disease in the adulthood, termed developmental origins of health and disease, has been increasingly recognized. With respect to the kidney, low birth weight is associated with a risk for hypertension and renal disease, and reduced nephron number is considered to be the cause. In animals, maternal protein or global nutrient restriction, uterine artery ligation, hyperglycemia, and exposure to various agents such as glucocorticoids or alcohol produce offspring with fewer nephrons (1-6). Depletion of stem cells by increased apoptosis has been suggested to be responsible for the decreased nephron formation (1,3). On the other hand, ureteric bud branching is a fundamental step in determining nephron number. The mechanism of reduced nephron endowment in dexamethasone or ethanol exposure has been suggested to be inhibited branching morphogenesis in an organ culture study (5,7). Reduced ureteric branching has recently been reported in a model of maternal hyperglycemia in vivo (8).Another possible mechanism of reduced nephron number is early cessation of nephrogenesis. In human premature infants, nephrogenesis is reported to continue only up to 40 d after birth (9). These infants are under various stresses including hypoxia, infection, and medications adversely affecting nephrogenesis. It has been postulated that adverse conditions during development promote differentiation aiming at early maturation and survival at the expense of reduced organ growth. Newborn rats resemble human premature neonates in that nephrogenesis continues after birth. Early cessation of nephrogenesis, therefore, may b...

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Section: Articlesmentioning

confidence: 99%

Maternal nutrient restriction inhibits ureteric bud branching but does not affect the duration of nephrogenesis in rats

Awazu

Hida

2015

Pediatr Res

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“…In 2004 three different groups published convergent results, showing that apoptotic cells of the wing imaginal discs release signaling molecules, namely wg and dpp, which promote cell proliferation in their vicinity (Huh et al 2004;Perez-Garijo et al 2004;Ryoo et al 2004). These results definitely provided a link between apoptosis and compensatory proliferation, and pointed to an active model involving the non-apoptotic functions of caspases (Kuranaga and Miura 2007;Fan and Bergmann 2008;Martin et al 2009). …”

Section: Apoptotic Cells Provide a Transient Source Of Signaling In Dmentioning

confidence: 60%

Injury-induced asymmetric cell death as a driving force for head regeneration in Hydra

Galliot

2012

Dev Genes Evol

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The freshwater Hydra polyp provides a unique model system to decipher the mechanisms underlying adult regeneration. Indeed a single cut initiates two distinct regenerative processes, foot regeneration on one side, head regeneration on the other side, the latter relying on the rapid formation of a local head organizer. Two aspects are discussed here, the asymmetric cellular remodeling induced by mid-gastric bisection and the signaling events that trigger head organizer formation. In head-regenerating tips (but not in foot ones) a wave of cell death takes place immediately, leading the apoptotic cells to transiently release Wnt3 and activate the β-catenin pathway in the neighboring cycling cells to push them through mitosis. This process, which mimics the apoptosis-induced compensatory proliferation process deciphered in Drosophila larvae regenerating their discs likely corresponds to an evolutionarily-conserved mechanism, also at work in Xenopus tadpoles regenerating their tale or mice regenerating their skin or liver. How is this process generated in Hydra? Several studies pointed to the necessary activation of the ERK 1-2 and MAPK pathways during early head regeneration and indeed ERK 1-2 inhibition or RSK, CREB, CBP knockdown prevent injury-induced apoptosis and head regeneration. The current scenario involves an asymmetric activation of the MAPK/CREB pathway to trigger injury-induced apoptosis in the interstitial cells, and, in the epithelial cells a CREB/CBP-dependent transcriptional activation of early genes essential for head organizing activity as wnt3, HyBra1, prdl-a. The question now is how bisection in the rather uniform central region of the polyp can generate this immediately asymmetric signaling.

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“…This leads to cleavage of their substrates and ultimately cell death through the programmed cell death pathway. The caspase family is essential not only for cell death, but also for immunity, neurogenesis, synaptic activity, cell proliferation and differentiation (D'Amelio, Cavallucci, and Cecconi 2010; Kuranaga and Miura 2007;Schwerk and Schulze-Osthoff 2003).…”

Section: Introductionmentioning

confidence: 99%

Organ-specific alteration in caspase expression and STK3 proteolysis during the aging process

Lessard‐Beaudoin

Laroche

Loudghi

et al. 2016

Neurobiology of Aging

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Caspases and their substrates are key mediators of apoptosis and strongly implicated in various physiological processes. As the STK family is involved in apoptosis, and STK3 is a recently identified caspase-6 substrate, we assessed the expression and cleavage of STK3 in murine peripheral organs and brain regions during the aging process. We also assessed caspase-3, -6, -7 and -8 expression and activity in order to delineate potential mechanism(s) underlying the generation of the STK3 fragments observed, and their relation to the apoptotic pathway. We demonstrate for the first time the cleavage of STK3 by caspase-7 and show that STK3 protein levels globally increase throughout the organism with age. In contrast, caspase-3, -6, -7 and -8 expression and activity vary significantly amongst the different organs analyzed suggesting differential effects of aging on the apoptotic mechanism and/or non-apoptotic functions of caspases throughout the organism. These results further our understanding of the role of caspases and their substrates in the normal aging process and highlight a potential role for STK3 in neurodegeneration.3

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Nonapoptotic functions of caspases: caspases as regulatory molecules for immunity and cell-fate determination

Cited by 167 publications

References 80 publications

Maternal nutrient restriction inhibits ureteric bud branching but does not affect the duration of nephrogenesis in rats

Maternal nutrient restriction inhibits ureteric bud branching but does not affect the duration of nephrogenesis in rats

Injury-induced asymmetric cell death as a driving force for head regeneration in Hydra

Organ-specific alteration in caspase expression and STK3 proteolysis during the aging process

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