Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2009-6-30
pubmed:abstractText
Skeletal muscle cells are exposed to mechanical stretch during embryogenesis. Increased stretch may contribute to cell death, and the molecular regulation by stretch remains incompletely understood. The aim of this study was to investigate the effects of cyclic stretch on cell death and apoptosis in myoblast using a Flexercell Strain Unit. Apoptosis was studied by annexin V binding and PI staining, DNA size analysis, electron microphotograph, and caspase assays. Fas/FasL expression was determined by Western blot. When myoblasts were cultured on a flexible membrane and subjected to cyclic strain stress, apoptosis was observed in a time-dependent manner. We also determined that stretch induced cleavage of caspase-3 and increased caspase-3 activity. Caspase-3 inhibition reduced stretch-induced apoptosis. Protein levels of Fas and FasL remained unchanged. Our findings implicated that stretch-induced cell death is an apoptotic event, and that the activation of caspase cascades is required in stretch-induced cell apoptosis. Furthermore, we had provided evidence that caspase-3 mediated cyclic stretch-induced myoblast apoptosis. Mechanical forces induced activation of caspase-3 via signaling pathways independent of Fas/FasL system.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1097-4644
pubmed:author
pubmed:copyrightInfo
2009 Wiley-Liss, Inc.
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
107
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
834-44
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Caspase-3-mediated cyclic stretch-induced myoblast apoptosis via a Fas/FasL-independent signaling pathway during myogenesis.
pubmed:affiliation
Department of Orthodontics, The Fourth Military Medical University, Xi'an, Shanxi Province, People's Republic of China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't