دورية أكاديمية

Early Developmental Disruption of Type 2 Deiodinase Pathway in Mouse Skeletal Muscle Does Not Impair Muscle Function.

التفاصيل البيبلوغرافية
العنوان: Early Developmental Disruption of Type 2 Deiodinase Pathway in Mouse Skeletal Muscle Does Not Impair Muscle Function.
المؤلفون: Ignacio DL; 1 Division of Endocrinology and Metabolism, Rush University Medical Center , Chicago, Illinois.; 2 Biophysics Institute and School of Physical Education and Sports, Federal University of Rio de Janeiro , Rio de Janeiro, Brazil ., Silvestre DH; 1 Division of Endocrinology and Metabolism, Rush University Medical Center , Chicago, Illinois.; 2 Biophysics Institute and School of Physical Education and Sports, Federal University of Rio de Janeiro , Rio de Janeiro, Brazil .; 3 Nutrition Institute Josué de Castro, Federal University of Rio de Janeiro , Rio de Janeiro, Brazil ., Anne-Palmer E; 1 Division of Endocrinology and Metabolism, Rush University Medical Center , Chicago, Illinois., Bocco BM; 1 Division of Endocrinology and Metabolism, Rush University Medical Center , Chicago, Illinois.; 4 Department of Translational Medicine, Federal University of São Paulo , São Paulo, Brazil ., Fonseca TL; 1 Division of Endocrinology and Metabolism, Rush University Medical Center , Chicago, Illinois., Ribeiro MO; 5 Developmental Disorders Program, Center for Biological and Health Sciences, Mackenzie Presbyterian University , São Paulo, Brazil ., Gereben B; 6 Department of Endocrine Neurobiology, Institute of Experimental Medicine , Hungarian Academy of Sciences, Budapest, Hungary ., Bianco AC; 1 Division of Endocrinology and Metabolism, Rush University Medical Center , Chicago, Illinois., Werneck-de-Castro JP; 1 Division of Endocrinology and Metabolism, Rush University Medical Center , Chicago, Illinois.; 2 Biophysics Institute and School of Physical Education and Sports, Federal University of Rio de Janeiro , Rio de Janeiro, Brazil .; 3 Nutrition Institute Josué de Castro, Federal University of Rio de Janeiro , Rio de Janeiro, Brazil .
المصدر: Thyroid : official journal of the American Thyroid Association [Thyroid] 2017 Apr; Vol. 27 (4), pp. 577-586. Date of Electronic Publication: 2017 Feb 10.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Mary Ann Liebert Publishers Country of Publication: United States NLM ID: 9104317 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1557-9077 (Electronic) Linking ISSN: 10507256 NLM ISO Abbreviation: Thyroid Subsets: MEDLINE
أسماء مطبوعة: Original Publication: New York, NY : Mary Ann Liebert Publishers,
مواضيع طبية MeSH: Iodide Peroxidase/*genetics , Muscle Development/*genetics , Muscle, Skeletal/*growth & development , Myoblasts/*metabolism , RNA, Messenger/*metabolism , Triiodothyronine/*metabolism, Animals ; Gene Expression Regulation, Developmental ; Mice ; Mice, Knockout ; Muscle, Skeletal/metabolism ; MyoD Protein/genetics ; Myogenic Regulatory Factor 5/genetics ; Myosin Heavy Chains/genetics ; Phenotype ; Sarcoplasmic Reticulum Calcium-Transporting ATPases/genetics ; Signal Transduction ; Iodothyronine Deiodinase Type II
مستخلص: Background: Myogenesis is positively regulated by thyroid hormone (triiodothyronine [T3]), which is amplified by the type 2 deiodinase (D2) activation of thyroxine to T3. Global inactivation of the Dio2 gene impairs skeletal muscle (SKM) differentiation and regeneration in response to muscle injury. Given that newborn and adult mice with late developmental SKM Dio2 disruption do not develop a significant phenotype, it was hypothesized that D2 plays an early role in this process.
Methods: This was tested in mice with SKM disruption of Dio2 driven by two early developmental promoters: MYF5 and MYOD.
Results: MYF5 myoblasts in culture differentiate normally into myotubes, despite loss of almost all D2 activity. Dio2 mRNA levels in developing SKM obtained from MYF5-D2KO embryos (E18.5) were about 54% of control littermates, but the expression of the T3-responsive genes Myh1 and 7 and Atp2a1 and 2 were not affected. In MYF5-D2KO and MYOD-D2KO neonatal hind-limb muscle, the expression of Myh1 and 7 and Atp2a2 remained unaffected, despite 60-70% loss in D2 activity and/or mRNA. Only in MYOD-D2KO neonatal muscle was there a 40% reduction in Atp2a1 mRNA. Postnatal growth of both mouse models and SKM function as assessed by exercise capacity and measurement of muscle strength were normal. Furthermore, an analysis of the adult soleus revealed no changes in the expression of T3-responsive genes, except for an about 18% increase in MYOD-D2KO SOL Myh7 mRNA.
Conclusion: Two mouse models of early developmental disruption of Dio2 in myocyte precursor exhibit no significant SKM phenotype.
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معلومات مُعتمدة: R01 DK077148 United States DK NIDDK NIH HHS
فهرسة مساهمة: Keywords: deiodinases; myogenesis; skeletal muscle function; thyroid hormone signaling
المشرفين على المادة: 0 (Myf5 protein, mouse)
0 (Myh7 protein, mouse)
0 (MyoD Protein)
0 (MyoD1 myogenic differentiation protein)
0 (Myogenic Regulatory Factor 5)
0 (RNA, Messenger)
06LU7C9H1V (Triiodothyronine)
EC 1.11.1.8 (Iodide Peroxidase)
EC 3.6.3.8 (Sarcoplasmic Reticulum Calcium-Transporting ATPases)
EC 3.6.4.1 (Myosin Heavy Chains)
EC 7.2.2.10 (Atp2a2 protein, mouse)
تواريخ الأحداث: Date Created: 20161215 Date Completed: 20180221 Latest Revision: 20231213
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC5385430
DOI: 10.1089/thy.2016.0392
PMID: 27967605
قاعدة البيانات: MEDLINE
الوصف
تدمد:1557-9077
DOI:10.1089/thy.2016.0392