CTG expansion and early proliferative arrest of DM1 myoblastes
Identifieur interne : 000021 ( Hal/Curation ); précédent : 000020; suivant : 000022CTG expansion and early proliferative arrest of DM1 myoblastes
Auteurs : Erwan Gasnier [France]Source :
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Abstract
Myotonic Dystrophy type I is the most common neuromuscular pathology at adult age. DM1 is characterized by a multisystemic but variable phenotype, correlated with the size of the CTG expansion. Skeletal muscle tissue is particularly affected showing myotonic symptoms and atrophy. Myoblasts, responsible for skeletal muscle growth and repair, present in DM1 patients a reduced proliferative capacity compared to cells isolated from non-affected individuals. During a previous study, p16INK4A was identified as the trigger of this abnormal proliferative arrest in DM1 myoblasts, but mechanisms activating this pathway are still unknown. In this study, we attempted to decrypt these mechanisms, particularly the potential links between CTG expansions, oxidative stress sensitivity and early activation of the p16 pathway leading to myoblasts senescence
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<front><div type="abstract" xml:lang="en">Myotonic Dystrophy type I is the most common neuromuscular pathology at adult age. DM1 is characterized by a multisystemic but variable phenotype, correlated with the size of the CTG expansion. Skeletal muscle tissue is particularly affected showing myotonic symptoms and atrophy. Myoblasts, responsible for skeletal muscle growth and repair, present in DM1 patients a reduced proliferative capacity compared to cells isolated from non-affected individuals. During a previous study, p16INK4A was identified as the trigger of this abnormal proliferative arrest in DM1 myoblasts, but mechanisms activating this pathway are still unknown. In this study, we attempted to decrypt these mechanisms, particularly the potential links between CTG expansions, oxidative stress sensitivity and early activation of the p16 pathway leading to myoblasts senescence</div>
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<abstract xml:lang="en">Myotonic Dystrophy type I is the most common neuromuscular pathology at adult age. DM1 is characterized by a multisystemic but variable phenotype, correlated with the size of the CTG expansion. Skeletal muscle tissue is particularly affected showing myotonic symptoms and atrophy. Myoblasts, responsible for skeletal muscle growth and repair, present in DM1 patients a reduced proliferative capacity compared to cells isolated from non-affected individuals. During a previous study, p16INK4A was identified as the trigger of this abnormal proliferative arrest in DM1 myoblasts, but mechanisms activating this pathway are still unknown. In this study, we attempted to decrypt these mechanisms, particularly the potential links between CTG expansions, oxidative stress sensitivity and early activation of the p16 pathway leading to myoblasts senescence</abstract>
<abstract xml:lang="fr">La dystrophie myotonique de type I est la pathologie neuromusculaire la plus répandue chez l'adulte. Elle est caractérisée par une atteinte multisystémique plus ou moins prononcée en fonction de l'extension des répétitions CTG, mutation à l'origine de l'atteinte. Le muscle squelettique est particulièrement touché avec un phénomène de myotonie ainsi qu'une atrophie. Les myoblastes, à l'origine de la formation des muscles et de leur régénération potentielle, présentent, chez les patients DM1, une capacité proliférative limitée par rapport à des myoblastes issus d'individus sains. C'est l'activation précoce de la voie p16 qui est à l'origine de cette sénescence prématurée des cellules DM1. Les mécanismes conduisant à ce phénotype sont néanmoins inconnus. Au cours de cette étude, nous avons tenté de décrypter une partie de ces mécanismes et notamment les liens potentiels entre les expansions CTG, la sensibilité au stress oxydatif et l'activation précoce de la voie p16 conduisant à la sénescence des myoblastes DM1</abstract>
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