Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1995-10-17
pubmed:abstractText
The purpose was to test hypotheses regarding the affect of thyroid hormone status on development of myosin heavy chain (MHC) protein phenotype in regenerating skeletal muscle. Soleus (SOL) and extensor digitorum longus (EDL) muscle grafts were studied 30 and 60 d following graft operations in eu-, hypo-, and hyperthyroid rats. Hyperthyroidism had a more profound affect on MHC phenotype than did hypothyroidism, and this was noted in SOL grafts more so than EDL grafts. For example, compared with euthyroid hosts at 30 d, SOL grafts from hyperthyroid hosts demonstrated a decrease from 83% to 3% in Type I MHC, and a decrease from 11% to 4% in Type IIa. Furthermore, Type IIx MHC increased from 5% to 12%, and Type IIb MHC increased from 3% to 82%. The change in Type I and IIb MHC noted at 30 d partially or fully reversed to euthyroid values by 60 d, whereas the hyperthyroid-induced differences in Type IIa and IIx were sustained. The adaptation of control muscles to hypo- and hyperthyroidism was qualitatively similar to muscle grafts for all MHC protein isoforms with the exception of Type IIx, which was expressed more so in grafts. For both grafts and control muscles, the adaptive response of MHC phenotype to sustained hyperthyroidism is transient for several of the MHC isoforms.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0195-9131
pubmed:author
pubmed:issnType
Print
pubmed:volume
27
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
674-81
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Myosin heavy chain phenotype in regenerating skeletal muscle is affected by thyroid hormone.
pubmed:affiliation
Department of Human Biodynamics, University of California, Berkeley 94720-4480, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't