Linked Life Data

2027030

Source:http://linkedlifedata.com/resource/pubmed/id/2027030

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1991-6-7
pubmed:abstractText
The glucocorticoid methylprednisolone (Mepd) increased dystrophin and myosin heavy chain levels in differentiated cultures of cloned human myoblasts. Mepd increased the number of myotubes per area by preventing myotube death and detachment during myogenesis in vitro. Myotube death was the result of an endogenous process initiated early during myoblast fusion. It occurred between days 4 and 5 of differentiation (3 days after its initiation) and was inhibited by cycloheximide, indicating that a programmed death mechanism may be involved. Inhibition of myotube death accounted for the increased levels of muscle-specific proteins; the amount of dystrophin per myonucleus was the same with or without Mepd treatment. These effects of glucocorticoids on primary muscle cultures may bear on the recent observation that prednisone transiently enhances muscle function in Duchenne muscular dystrophy.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0022-510X
pubmed:author
pubmed:issnType
Print
pubmed:volume
101
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
73-81
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Methylprednisolone increases dystrophin levels by inhibiting myotube death during myogenesis of normal human muscle in vitro.
pubmed:affiliation
Cecil B. Day Neuromuscular Research Laboratories, Massachusetts General Hospital, Charlestown 02129.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't