Concise Review: Quiescence in Adult Stem Cells: Biological Significance and Relevance to Tissue Regeneration

Rumman, Mohammad; Dhawan, Jyotsna; Kassem, Moustapha

doi:10.1002/stem.2056

Cited by 139 publications

(133 citation statements)

References 98 publications

Supporting

Mentioning

124

Contrasting

Unclassified

Order By: Relevance

“…The reactivation of qNSCs into proliferation is crucial for tissue repair and regeneration. This reactivation not only exists in neural stem cells, but it also occurs in other tissue stem cells such as fibroblasts and hematopoietic stem cells (Rumman et al, 2015). Studies in the past few years have revealed that, instead of being a passive state, quiescence is actively maintained in the cell (Spencer et al, 2013; Hilpert et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Traumatic Brain Injury Stimulates Neural Stem Cell Proliferation via Mammalian Target of Rapamycin Signaling Pathway Activation

Wang

Seekaew

Gao

et al. 2016

eNeuro

View full text Add to dashboard Cite

Neural stem cells in the adult brain possess the ability to remain quiescent until needed in tissue homeostasis or repair. It was previously shown that traumatic brain injury (TBI) stimulated neural stem cell (NSC) proliferation in the adult hippocampus, indicating an innate repair mechanism, but it is unknown how TBI promotes NSC proliferation. In the present study, we observed dramatic activation of mammalian target of rapamycin complex 1 (mTORC1) in the hippocampus of mice with TBI from controlled cortical impact (CCI). The peak of mTORC1 activation in the hippocampal subgranular zone, where NSCs reside, is 24–48 h after trauma, correlating with the peak of TBI-enhanced NSC proliferation. By use of a Nestin-GFP transgenic mouse, in which GFP is ectopically expressed in the NSCs, we found that TBI activated mTORC1 in NSCs. With 5-bromo-2′-deoxyuridine labeling, we observed that TBI increased mTORC1 activation in proliferating NSCs. Furthermore, administration of rapamycin abolished TBI-promoted NSC proliferation. Taken together, these data indicate that mTORC1 activation is required for NSC proliferation postinjury, and thus might serve as a therapeutic target for interventions to augment neurogenesis for brain repair after TBI.

show abstract

Section: Discussionmentioning

confidence: 99%

Traumatic Brain Injury Stimulates Neural Stem Cell Proliferation via Mammalian Target of Rapamycin Signaling Pathway Activation

Wang

Seekaew

Gao

et al. 2016

eNeuro

View full text Add to dashboard Cite

show abstract

“…MuSCs are quiescent (G 0 phase) during homeostasis (Rumman et al, 2015;Schultz et al, 1978). Following injury, they re-enter the cell cycle, proliferate to give rise to myoblasts that differentiate and fuse to restore the damaged fibre or generate myofibres de novo (Moss and Leblond, 1970;Reznik, 1969;Snow, 1977).…”

Section: Morel Et Al 2007)mentioning

confidence: 99%

Regulation and phylogeny of skeletal muscle regeneration

Baghdadi

Tajbakhsh

2018

Developmental Biology

158

135

View full text Add to dashboard Cite

One of the most fascinating questions in regenerative biology is why some animals can regenerate injured structures while others cannot. Skeletal muscle has a remarkable capacity to regenerate even after repeated traumas, yet limited information is available on muscle repair mechanisms and how they have evolved. For decades, the main focus in the study of muscle regeneration was on muscle stem cells, however, their interaction with their progeny and stromal cells is only starting to emerge, and this is crucial for successful repair and reestablishment of homeostasis after injury. In addition, numerous murine injury models are used to investigate the regeneration process, and some can lead to discrepancies in observed phenotypes. This review addresses these issues and provides an overview of the some of the main regulatory cellular and molecular players involved in skeletal muscle repair.Key words: skeletal muscle, regeneration, stem cells, evolution, quiescence, injury IntroductionThe ability to regenerate tissues and structures is a prevalent feature of metazoans although there is significant variability among species ranging from limited regeneration of a tissue (birds and mammals) to regeneration involving the entire organism (cnidarians, planarians, hydra). The intriguing evolutionary loss of regenerative capacity in more complex organisms highlights the importance of identifying the underlying mechanisms responsible for these diverse regenerative strategies. One of the most studied tissues that contributes to new appendage formation is skeletal muscle, thereby making it a major focus of regeneration studies during evolution. The emergence of new lineage-tracing tools in different animal models has permitted the identification of specific progenitor cell populations and their contribution to tissue repair.Skeletal muscles allow voluntary movement and they play a key role in regulating metabolism and homeostasis in the organism. In mice and humans this tissue represents about 30-40% of the total body mass. This tissue provides an excellent tractable model to study regenerative myogenesis and the relative roles of stem and stromal cells following a single, or repeated rounds of injury. Although muscle regeneration relies mainly on its resident muscle stem (satellite) cells (MuSCs) to effect muscle repair, interactions with neighbouring stromal cells, by direct contact or via the release of soluble factors, is essential to restore proper 3 function. Each step of the myogenic process is regulated by specific regulatory factors including extrinsic cues, yet the nature and source of these signals remain unclear. This review will address these issues and discuss the different experimental models used to investigate the regenerative process. Prenatal and postnatal skeletal muscle developmentIn amniotes, skeletal muscles in the limbs and trunk arise from somites through a series of successive waves that include embryonic and foetal phases of myoblast production (Biressi et al., 2007;Comai and Tajbakhsh, 201...

show abstract

“…Cumulative studies have shown that maintenance of SC quiescence in a number of SCs such as hematopoietic SCs, muscle satellite cells, and skeletal mesenchymal SCs is clinically relevant for enhancing tissue regeneration. 7 …”

Section: Introductionmentioning

confidence: 99%

Niche Regulation of Limbal Epithelial Stem Cells: Relationship between Inflammation and Regeneration

Tseng

Zhang

et al. 2016

The Ocular Surface

View full text Add to dashboard Cite

Human limbal palisades of Vogt are the ideal site for studying and practicing regenerative medicine due to their accessibility. Nonresolving inflammation in limbal stroma is common manifestation of limbal stem cell (SC) deficiency and presents as a threat to the success of transplanted limbal epithelial SCs. This pathologic process can be overcome by transplantation of cryopreserved human amniotic membrane (AM), which exerts anti-inflammatory, antiscarring and anti-angiogenic action to promote wound healing. To determine how AM might exert anti-inflammation and promote regeneration, we have purified a novel matrix, HC-HA/PTX3, responsible for the efficacy of AM efficacy. HC-HA complex is covalently formed by hyaluronan (HA) and heavy chain 1 (HC1) of inter-α-trypsin inhibitor by the catalytic action of tumor necrosis factor-stimulated gene-6 (TSG-6) and are tightly associated with pentraxin 3 (PTX3) to form HC-HA/PTX3. In vitro reconstitution of the limbal niche can be established by reunion between limbal epithelial progenitors and limbal niche cells on different substrates. In 3-dimensional Matrigel, clonal expansion indicative of SC renewal is correlated with activation of canonical Wnt signaling and suppression of canonical BMP signaling. In contrast, SC quiescence can be achieved in HC-HA/PTX3 by activation of canonical BMP signaling and non-canonical planar cell polarity (PCP) Wnt signaling, but suppression of canonical Wnt signaling. HC-HA/PTX3 is a novel matrix mitigating nonresolving inflammation and restoring SC quiescence in the niche for various applications in regenerative medicine.

show abstract

Concise Review: Quiescence in Adult Stem Cells: Biological Significance and Relevance to Tissue Regeneration

Cited by 139 publications

References 98 publications

Traumatic Brain Injury Stimulates Neural Stem Cell Proliferation via Mammalian Target of Rapamycin Signaling Pathway Activation

Traumatic Brain Injury Stimulates Neural Stem Cell Proliferation via Mammalian Target of Rapamycin Signaling Pathway Activation

Regulation and phylogeny of skeletal muscle regeneration

Niche Regulation of Limbal Epithelial Stem Cells: Relationship between Inflammation and Regeneration

Contact Info

Product

Resources

About