NDLI: Premature senescence in primary muscle cultures of myotonic dystrophy type 2 is not associated with p16 induction.

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Premature senescence in primary muscle cultures of myotonic dystrophy type 2 is not associated with p16 induction.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Renna, L. V. Cardani, R. Botta, A. Rossi, G. Fossati, B. Costa, E. Meola, G.
Description	Author Affiliation: Renna LV ( University of Milan. laura.renna@unimi.it.)
Abstract	Myotonic dystrophy type 1 (DM1) and type 2 (DM2) are multisystemic disorders linked to two different genetic loci and characterized by several features including myotonia, muscle weakness and atrophy, cardiac dysfunctions, cataracts and insulin-resistance. In both forms, expanded nucleotide sequences cause the accumulation of mutant transcripts in the nucleus deregulating the activity of some RNAbinding proteins and providing an explanation for the multisystemic phenotype of DM patients. However this pathogenetic mechanism does not explain some histopathological features of DM skeletal muscle like muscle atrophy. It has been observed that DM muscle shares similarities with the ageing muscle, where the progressive muscle weakness and atrophy is accompanied by a lower regenerative capacity possibly due to the failure in satellite cells activation. The aim of our study is to investigate if DM2 satellite cell derived myoblasts exhibit a premature senescence as reported for DM1 and if alterations in their proliferation potential and differentiation capabilities might contribute to some of the histopathological features observed in DM2 muscles. Our results indicate that DM myoblasts have lower proliferative capability than control myoblasts and reach in vitro senescence earlier than controls. Differentely from DM1, the p16 pathway is not responsible for the premature growth arrest observed in DM2 myoblasts which stop dividing with telomeres shorter than controls. During in vitro senescence, a progressive decrease in fusion index is observable in both DM and control myotubes with no significant differences between groups. Moreover, myotubes obtained from senescent myoblasts appear to be smaller than those from young myoblasts. Taken together, our data indicate a possible role of DM2 premature myoblast senescence in skeletal muscle histopathological alterations i.e., dystrophic changes and type 2 fibre atrophy.
File Format	HTM / HTML
ISSN	1121760X
e-ISSN	20388306
DOI	10.4081/ejh.2014.2444
Journal	European Journal of Histochemistry
Issue Number	4
Volume Number	58
Language	English
Publisher	PagePress
Publisher Date	2014-10-22
Publisher Place	Italy
Access Restriction	Open
Subject Keyword	Discipline Histocytochemistry Cell Aging Cyclin-dependent Kinase Inhibitor P16 Biosynthesis Gene Expression Regulation Muscle Fibers, Skeletal Metabolism Muscle Proteins Myotonic Dystrophy Cells, Cultured Pathology Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Cell Biology Histology Biophysics

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Premature Senescence in Primary Muscle Cultures of Myotonic Dystrophy Type 2 is not Associated with p16 Induction

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Premature senescence in primary muscle cultures of myotonic dystrophy type 2 is not associated with p16 induction.