Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1994-1-31
pubmed:abstractText
Using muscle as an in vivo model system, we have tested the hypothesis that basic fibroblast growth factor is released from a cytoplasmic storage site into the extra-cellular environment via diffusion through survivable, mechanically-induced plasma membrane disruptions. Normal and dystrophic (mdx) mouse muscle were studied. Strong immunostaining for bFGF was detected in the cytoplasm of myofibers of uninjured muscle fixed in situ by perfusion. By contrast, myofibers did not stain cytoplasmically for bFGF after suffering lethal disruptions of their plasma membranes caused by freezing and thawing followed by sectioning. Sub-lethal, transient disruptions of myofiber plasma membranes--termed plasma membrane 'wounds'--were shown to be induced by needle puncture or exercise of muscle. Quantitative image analysis revealed that these wounded fibers contained significantly reduced levels of bFGF. Dystrophic exercised and unexercised muscle was found to possess an approximately 6-fold higher proportion of wounded myofibers than does normal muscle under equivalent conditions. Release of bFGF at a rate that is a direct function of the frequency of myofiber wounding may explain in part how a muscle adjusts its growth to meet changing mechanical demand as well as the pathological hypertrophy characteristic of certain stages of muscular dystrophy.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0021-9533
pubmed:author
pubmed:issnType
Print
pubmed:volume
106 ( Pt 1)
pubmed:geneSymbol
mdx
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
121-33
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Loss of cytoplasmic basic fibroblast growth factor from physiologically wounded myofibers of normal and dystrophic muscle.
pubmed:affiliation
Department of Anatomy and Cellular Biology, Harvard Medical School, Boston, MA 02115.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't