The Regulation of Notch Signaling Controls Satellite Cell Activation and Cell Fate Determination in Postnatal Myogenesis

Conboy, Irina M.; Rando, Thomas A.

doi:10.1016/s1534-5807(02)00254-x

Cited by 776 publications

(833 citation statements)

References 44 publications

(2 reference statements)

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“…Concerning the latter, satellite cells are the main contributor to muscle maintenance, growth and repair (Anderson and Wozniak 2004). Thus, a decline in the number of satellite cells (Kadi et al 2004;Renault et al 2002;Verdijk et al 2007) or their inability to become active and proliferate in response to anabolic stimuli (Conboy et al 2003;Conboy and Rando 2002) may contribute to the development of sarcopenia.…”

Section: Sarcopenia In the Elderly: A Common Problemmentioning

confidence: 99%

Genes and the ageing muscle: a review on genetic association studies

Garatachea

Lucía

2011

AGE

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Western populations are living longer. Ageing decline in muscle mass and strength (i.e. sarcopenia) is becoming a growing public health problem, as it contributes to the decreased capacity for independent living. It is thus important to determine those genetic factors that interact with ageing and thus modulate functional capacity and skeletal muscle phenotypes in older people. It would be also clinically relevant to identify 'unfavourable' genotypes associated with accelerated sarcopenia. In this review, we summarized published information on the potential associations between some genetic polymorphisms and muscle phenotypes in older people. A special emphasis was placed on those candidate polymorphisms that have been more extensively studied, i.e. angiotensinconverting enzyme (ACE) gene I/D, α-actinin-3 (ACTN3) R577X, and myostatin (MSTN) K153R, among others. Although previous heritability studies have indicated that there is an important genetic contribution to individual variability in muscle phenotypes among old people, published data on specific gene variants are controversial. The ACTN3 R577X polymorphism could influence muscle function in old women, yet there is controversy with regards to which allele (R or X) might play a 'favourable' role. Though more research is needed, up-to-date MSTN genotype is possibly the strongest candidate to explain variance among muscle phenotypes in the elderly. Future studies should take into account the association between muscle phenotypes in this population and complex gene-gene and gene-environment interactions.

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Section: Sarcopenia In the Elderly: A Common Problemmentioning

confidence: 99%

Genes and the ageing muscle: a review on genetic association studies

Garatachea

Lucía

2011

AGE

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“…Soluble factors such as BMPs (Xie and Spradling, 1998;Kobielak et al, 2003;Zhang et al, 2003;Andl et al, 2004;He et al, 2004;Yamashita et al, 2005), FGFs (Kashiwakura and Takahashi, 2005), Shh (Madison et al, 2005;Crosnier et al, 2006), and Wnts (Gat et al, 1998;Korinek et al, 1998;Huelsken et al, 2001;Niemann et al, 2002;Reya et al, 2003;Willert et al, 2003) are present within the niche and can originate from support cells, stem cells themselves, or differentiated cell. Cell-to-cell contact-mediated signaling is also present in adult niches in the form of connexins (Juneja et al, 1999;Plum et al, 2000), ephrins/eph (Batlle et al, 2002;Holmberg et al, 2006) and Notch (Harada et al, 1999;Lowell et al, 2000;Conboy and Rando, 2002;Calvi et al, 2003;Conboy et al, 2003;Kumano et al, 2003;Tummers and Thesleff, 2003;Hadland et al, 2004;Fre et al, 2005;Robert-Moreno et al, 2005;van Es et al, 2005;Spradling, 2006, 2007;Song et al, 2007). These signaling mechanisms may occur between stem cells, between support cells and stem cells, and between stem cells and differentiating cells.…”

Section: Introductionmentioning

confidence: 99%

The microenvironment of the embryonic neural stem cell: Lessons from adult niches?

Lathia

Rao

Mattson

et al. 2007

Developmental Dynamics

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A better understanding of the signals regulating embryonic neural stem cells is clearly an important goal. However, many studies on neural stem cell biology are conducted on the slowly-dividing cells found in the adult CNS, where specialized microenvironments or niches maintain the stem cells throughout life. By contrast, the embryonic VZ is a transient structure that does not fulfill the criteria conventionally used to define niches. In this review we will examine whether, despite these differences, the signals found in other adult stem cell niches are present in the VZ. Using the similarities and differences we observe, we will reconsider whether the location of embryonic stem cell populations such as the VZ can be thought of as niches. Finally, we will ask how these lessons from the niche inform our understanding of neurodevelopmental diseases and cancers of the CNS. Developmental Dynamics 236:3267-3282, 2007.

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“…Activation of contractile protein genes is dependent upon myoD in skeletal muscle development (Weintraub, 1993;Cornelison and Wold, 1997;Conboy and Rando, 2002). The spatio-temporal pattern of titin localization noted above indicates that it expressed early in the differentiation of nascent myotomal myoblast cells.…”

Section: Spatio-temporal Relationship Between Myod and Titin Expressionmentioning

confidence: 91%

The pattern of MyoD and contractile protein localization in primary epaxial myotome reflects the dynamic progression of nascent myoblast differentiation

Yang

Ordahl

2005

Developmental Dynamics

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The localization of contractile and regulatory proteins in early stages of epaxial primary myotome development was analyzed by immunofluorescence microscopy. Contractile proteins that appear in an ordered sequence in the rostro-caudal axis of somite development were found to reiterate that sequence in the dorso-medial-to-ventro-lateral axis of primary epaxial myotome development. Pair-wise localization of MyoD-titin, desmin-titin, and desmin-myosin defined three zones extending from the dermomyotome dorso-medial lip (DML) into the primary myotome layer. Zones M1 and M2, which were positive for MyoD ؉ titin and MyoD ؉ titin ؉ desmin, respectively, were restricted to the dorso-medial-most extremity of the myotome layer and did not expand during the course of myotome development. Zone M3 was positive for MyoD, desmin, titin, myosin, and cardiac troponin T and was the only zone that expanded during primary myotome development. Myotome fibers in zone M3 were unit-length, spanning the full rostro-caudal axis of the myotome while fibers in zones M1 and M2 were shorter than unit length. Anti-myoD immunofluorescence, when detected in cells lacking contractile-protein-positive cytoplasm, was restricted to the DML and nascent myotome cells immediately subjacent to the DML. These results demonstrate a dynamic spatiotemporal sequence in the differentiation program of nascent myotome cells as they emerge from the DML; zones M1 and M2 reflect standing waves of sequential contractile protein activation during the maturation of nascent myotomal myoblasts, while the expanding zone M3 reflects the accumulation of mature myotome fibers expressing a full cohort contractile proteins. Developmental Dynamics 235:382-394, 2006.

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The Regulation of Notch Signaling Controls Satellite Cell Activation and Cell Fate Determination in Postnatal Myogenesis

Cited by 776 publications

References 44 publications

Genes and the ageing muscle: a review on genetic association studies

Genes and the ageing muscle: a review on genetic association studies

The microenvironment of the embryonic neural stem cell: Lessons from adult niches?

The pattern of MyoD and contractile protein localization in primary epaxial myotome reflects the dynamic progression of nascent myoblast differentiation

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