Thyroid hormone signaling in male mouse skeletal muscle is largely independent of D2 in myocytes

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dc.contributor.authorWerneck-De-Castro J.P.
dc.contributor.authorFonseca T.L.
dc.contributor.authorIgnacio D.L.
dc.contributor.authorFernandes G.W.
dc.contributor.authorAndrade-Feraud C.M.
dc.contributor.authorLartey L.J.
dc.contributor.authorRibeiro M.B.
dc.contributor.authorRibeiro M.O.
dc.contributor.authorGereben B.
dc.contributor.authorBianco A.C.
dc.date.accessioned2024-03-13T00:56:14Z
dc.date.available2024-03-13T00:56:14Z
dc.date.issued2015
dc.description.abstract© 2015 by the Endocrine Society.The type 2 deiodinase (D2) activates the prohormone T4 to T3.D2 is expressed in skeletal muscle (SKM), and its global inactivation (GLOB-D2KO mice) reportedly leads to skeletal muscle hypothyroidism and impaired differentiation. Here floxed Dio2 mice were crossed with mice expressing Cre-recombinase under the myosin light chain 1f (cre-MLC) to disrupt D2 expression in the late developmental stages of skeletal myocytes (SKM-D2KO). This led to a loss of approximately 50% in D2 activity in neonatal and adult SKM-D2KO skeletal muscle and about 75% in isolated SKM-D2KO myocytes. To test the impact of Dio2 disruption, we measured soleus T3 content and found it to be normal. We also looked at the expression of T3-responsive genes in skeletal muscle, ie, myosin heavy chain I, α-actin, myosin light chain, tropomyosin, and serca 1 and 2, which was preserved in neonatal SKM-D2KO hindlimb muscles, at a time that coincides with a peak of D2 activity in control animals. In adult soleus the baseline level of D2 activity was about 6-fold lower, and in the SKM-D2KO soleus, the expression of only one of five T3-responsive genes was reduced. Despite this, adult SKM-D2KO animals performed indistinguishably from controls on a treadmill test, running for approximately 16 minutes and reached a speed of about 23m/min;musclestrengthwasabout0.3mN/m-gbodyweightinSKM-D2KOandcontrolanklemuscles. In conclusion, there are multiple sources of D2 in the mouse SKM, and its role is limited in postnatal skeletal muscle fibers.
dc.description.firstpage3842
dc.description.issuenumber10
dc.description.lastpage3852
dc.description.volume156
dc.identifier.doi10.1210/en.2015-1246
dc.identifier.issn1945-7170
dc.identifier.urihttps://dspace.mackenzie.br/handle/10899/36144
dc.relation.ispartofEndocrinology
dc.rightsAcesso Aberto
dc.titleThyroid hormone signaling in male mouse skeletal muscle is largely independent of D2 in myocytes
dc.typeArtigo
local.scopus.citations22
local.scopus.eid2-s2.0-84943597432
local.scopus.subjectAdipose Tissue, Brown
local.scopus.subjectAnimals
local.scopus.subjectAnimals, Newborn
local.scopus.subjectCells, Cultured
local.scopus.subjectGene Expression
local.scopus.subjectIodide Peroxidase
local.scopus.subjectMale
local.scopus.subjectMice, Knockout
local.scopus.subjectMice, Transgenic
local.scopus.subjectMuscle Fibers, Skeletal
local.scopus.subjectMuscle Strength
local.scopus.subjectMuscle, Skeletal
local.scopus.subjectMyosin Heavy Chains
local.scopus.subjectPhysical Conditioning, Animal
local.scopus.subjectReverse Transcriptase Polymerase Chain Reaction
local.scopus.subjectSarcoplasmic Reticulum Calcium-Transporting ATPases
local.scopus.subjectSignal Transduction
local.scopus.subjectThyroid Hormones
local.scopus.subjectThyroxine
local.scopus.subjectTime Factors
local.scopus.subjectTriiodothyronine
local.scopus.subjectTropomyosin
local.scopus.updated2024-05-01
local.scopus.urlhttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84943597432&origin=inward
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