Effect of aging on stem cells

Ahmed, Abu; Sheng, Matilda H.‐C.; Wasnik, Samiksha; Baylink, David J.; Lau, K.-H. William

doi:10.5493/wjem.v7.i1.1

Cited by 159 publications

(99 citation statements)

References 142 publications

(138 reference statements)

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“…On the one hand, stimulation of proliferation of quiescent cells provokes the exhaustion of stem cells (Li & Clevers, 2010). On the other, the degenerative processes in stem cells and the systemic cues that regulate their activity have been connected to the agedependent decline in regenerative potential of tissues (Ahmed, , Wasnik, Baylink, & Lau, 2017). Proliferative potential of stem cells is reduced over time in quiescence.…”

Section: Discussionmentioning

confidence: 99%

Prolonged quiescence delays somatic stem cell‐like divisions in Caenorhabditis elegans and is controlled by insulin signaling

et al. 2019

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Cells can enter quiescence in adverse conditions and resume proliferation when the environment becomes favorable. Prolonged quiescence comes with a cost, reducing the subsequent speed and potential to return to proliferation. Here, we show that a similar process happens during Caenorhabditis elegans development, providing an in vivo model to study proliferative capacity after quiescence. Hatching under starvation provokes the arrest of blast cell divisions that normally take place during the first larval stage (L1). We have used a novel method to precisely quantify each stage of postembryonic development to analyze the consequences of prolonged L1 quiescence. We report that prolonged L1 quiescence delays the reactivation of blast cell divisions in C. elegans, leading to a delay in the initiation of postembryonic development. The transcription factor DAF-16/FOXO is necessary for rapid recovery after extended arrest, and this effect is independent from its role as a suppressor of cell proliferation. Instead, the activation of DAF-16 by decreased insulin signaling reduces the rate of L1 aging, increasing proliferative potential. We also show that yolk provisioning affects the proliferative potential after L1 arrest modulating the rate of L1 aging, providing a possible mechanistic link between insulin signaling and the maintenance of proliferative potential. Furthermore, variable yolk provisioning in embryos is one of the sources of interindividual variability in recovery after quiescence of genetically identical animals. Our results support the relevance of L1 arrest as an in vivo model to study stem cell-like aging and the mechanisms for maintenance of proliferation potential after quiescence. K E Y W O R D Sarrest, C. elegans, development, insulin signaling, proliferation, quiescence

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Section: Discussionmentioning

confidence: 99%

Prolonged quiescence delays somatic stem cell‐like divisions in Caenorhabditis elegans and is controlled by insulin signaling

et al. 2019

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“…The influence of various comorbidities on the exhaustion of MSCs has been studied intensively. Aging causes significant suppression of the osteogenic potential of MSCs and directs cell differentiation toward adipogenesis . The lower osteogenic potential of exhausted MSCs is associated with reduced reaction to HO‐promoting factors and a smaller volume of HO.…”

Section: Molecular Mechanisms In Heterotopic Ossificationmentioning

confidence: 99%

“…Not only aging but also obesity, a high‐fat diet, and type‐2 diabetes affect the function of MSCs. Hyperglycaemia and hyperinsulinaemia influence the microenvironment of the MSC niche, causing MSC exhaustion and dysfunction and reducing osteogenic differentiation . However, intensified adipogenesis increases the concentration of leptin, which regulates bone formation and can support osteogenesis .…”

Section: Molecular Mechanisms In Heterotopic Ossificationmentioning

confidence: 99%

Challenges of heterotopic ossification—Molecular background and current treatment strategies

Łęgosz

Drela

Pulik

et al. 2018

Clin Exp Pharma Physio

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Heterotopic ossification (HO) is an abnormal formation of mature lamellar bone within extraskeletal soft tissues, such as muscles, tendons, and ligaments. This process is thought to be induced by inflammation associated with tissue injuries. HO is classified using two subtypes: resulting from injury or genetically inherited. HO formation is associated with polytrauma patients with traumatic brain injuries and spinal cord injuries. Moreover, HO is also considered to be a post-operative risk factor in some orthopaedic procedures. In this review, we summarize our current understanding of the pathology of different types of HO and discuss its current and future therapies. Thus far, research has revealed cellular and molecular pathways leading to HO formation and proposed several possible mechanisms leading to HO and conserved signalling pathways common in the different HO subtypes. Non-steroidal anti-inflammatory drug treatment and localized low-dose irradiation are currently the only available prophylactic treatments for HO. However, they are not always effective and do not target the osteogenic processes directly. New therapeutic strategies targeting the pathological processes of HO, such as bone morphogenetic protein (BMP) inhibitors like noggin, BMP type 1 receptor inhibitor, and nuclear retinoid acid receptor-gamma (RARγ) agonists, are currently being investigated. In-depth understanding of the HO pathological process could help to develop effective therapeutic strategies.

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“…On the one hand, stimulation of proliferation of quiescent cells provokes the exhaustion of stem cells 29 . On the other, the degenerative processes in stem cells and the systemic cues that regulate their activity have been connected to the age-dependent decline in regenerative potential of tissues 30 . Proliferative potential of stem cells is reduced over time in quiescence.…”

Section: Resultsmentioning

confidence: 99%

Prolonged quiescence delays somatic stem cell-like division inCaenorhabditis elegansand is controlled by insulin signalling

Olmedo

Mata‐Cabana

Rodríguez-Palero

et al. 2018

Preprint

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Cells can enter quiescence in adverse conditions and resume proliferation when the environment becomes favorable. Prolonged quiescence comes with a cost, reducing the subsequent speed and potential to return to proliferation. Here, we show that a similar process happens during Caenorhabditis elegans development, providing an in vivo model to study proliferative capacity after quiescence. Hatching under starvation provokes the arrest of blast cell divisions that normally take place during the first larval stage (L1). We have used a novel method to precisely quantify each stage of postembryonic development to analyze the consequences of prolonged L1 quiescence. We report that prolonged L1 quiescence delays the reactivation of blast cell divisions in C. elegans, leading to a delay in the initiation of postembryonic development. The transcription factor DAF‐16/FOXO is necessary for rapid recovery after extended arrest, and this effect is independent from its role as a suppressor of cell proliferation. Instead, the activation of DAF‐16 by decreased insulin signaling reduces the rate of L1 aging, increasing proliferative potential. We also show that yolk provisioning affects the proliferative potential after L1 arrest modulating the rate of L1 aging, providing a possible mechanistic link between insulin signaling and the maintenance of proliferative potential. Furthermore, variable yolk provisioning in embryos is one of the sources of interindividual variability in recovery after quiescence of genetically identical animals. Our results support the relevance of L1 arrest as an in vivo model to study stem cell‐like aging and the mechanisms for maintenance of proliferation potential after quiescence.

show abstract

Effect of aging on stem cells

Cited by 159 publications

References 142 publications

Prolonged quiescence delays somatic stem cell‐like divisions in Caenorhabditis elegans and is controlled by insulin signaling

Prolonged quiescence delays somatic stem cell‐like divisions in Caenorhabditis elegans and is controlled by insulin signaling

Challenges of heterotopic ossification—Molecular background and current treatment strategies

Prolonged quiescence delays somatic stem cell-like division inCaenorhabditis elegansand is controlled by insulin signalling

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