Thyroid hormones regulate expression of the neural cell adhesion molecule in adult skeletal muscle

Thompson, Joanne; Moore, Stephen E.; Walsh, Frank S.

doi:10.1016/0014-5793(87)81205-x

Cited by 23 publications

(7 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Several thyroid hormone regulated genes have been identified in vivo in skeletal muscle. These include several members of the M H C gene family (Izumo et al 1986, Gustafson et al 1987, the Ca2+-ATPase of the sarcoplasmic reticulum (Simonides et al 1990) and the neural adhesive molecule (Thompson et al 1987). T, regulates the cellular expression of several muscle-specific proteins by T, receptormediated changes in the transcription of T,responsive genes (Flink & Morkin 1990, Izumo & Mahdavi 1988.…”

Section: Discussionmentioning

confidence: 99%

Thyroid hormone regulation of myosin heavy chain isoform composition in young and old rats, with special reference to IIX myosin

Larsson

Müller

et al. 1995

Acta Physiologica Scandinavica

View full text Add to dashboard Cite

The effects of 4 weeks of thyroid hormone (3,5,3'-triiodothyronine, T3) treatment on the myosin heavy chain (MHC) composition were compared in the slow-twitch soleus and the fast-twitch extensor digitorum longus (EDL) muscles from young (3-6 months) and old (20-24 months) male albino rats. Four MHC isoforms were separated on silver-stained 6% sodium dodecyl sulphate polyacrylamide gel electrophoresis. According to immunoblotting experiments with specific MHC monoclonal antibodies, the four MHCs corresponded to types I, IIB, IIX and IIA. In the soleus, the type I MHC content was higher in the old than in the young animals, and the type IIA content lower. Type IIX myosin was observed in some young control soleus, but not in old ones. After T3 treatment, the content of type I MHC decreased substantially in both young and old animals and that of type IIA increased. After T3 treatment, type IIX myosin was observed in both young and old animals, with a slightly higher IIX myosin content in old age, but the age-related difference in the contents of types I and IIA was diminished. In EDL, the type IIX MHC content was significantly higher in the old animals, at the expense of a lower content of type IIB MHC. MHC composition was not affected significantly by T3 treatment in EDL, either in young or old animals. In conclusion, an age-related motor unit transformation is observed in both the slow-twitch soleus and the fast-twitch EDL and the capacity for MHC isoform switching in response to T3 treatment is not impaired in old age.

show abstract

Section: Discussionmentioning

confidence: 99%

Thyroid hormone regulation of myosin heavy chain isoform composition in young and old rats, with special reference to IIX myosin

Larsson

Müller

et al. 1995

Acta Physiologica Scandinavica

View full text Add to dashboard Cite

show abstract

“…In addition, cyclic AMP and retinoic acid control NCAM expression in cultured cells (Husmann et al, 1989;Gegelashvili et al, 1993). In two other biological systems NCAM expression has been found to be under thyroid control: Xenopus laevis metamorphosis, where thyroxine induces NCAM in liver (Levi et al, 1990), and the adult rat skeletal muscle, where hypothyroidism causes the re-induction of NCAM (Thompson et al, 1987). As a result of a differential screening, a slight increase in the NCAM RNA content in the hypothyroid brain was previously reported (Munioz et al, 1991).…”

Section: Discussionmentioning

confidence: 93%

“…The reduced magnitude of this effect was probably due to the analysis of total cerebrum instead of the cerebral cortex, as in the present study. In two other biological systems NCAM expression has been found to be under thyroid control: Xenopus laevis metamorphosis, where thyroxine induces NCAM in liver (Levi et al, 1990), and the adult rat skeletal muscle, where hypothyroidism causes the re-induction of NCAM (Thompson et al, 1987). Interestingly, NCAM expression is also elevated in the peripheral nervous system of MAG-'mice (Montag et al, 1994), perhaps as a compensatory mechanism.…”

Section: Discussionmentioning

confidence: 99%

Thyroid hormone-dependent transcriptional repression of neural cell adhesion molecule during brain maturation.

et al. 1996

View full text Add to dashboard Cite

Thyroid hormone (T3) is a main regulator of brain development acting as a transcriptional modulator. However, only a few T3‐regulated brain genes are known. Using an improved whole genome PCR approach, we have isolated seven clones encoding sequences expressed in neonatal rat brain which are under the transcriptional control of T3. Six of them, including the neural cell adhesion molecule NCAM, alpha‐tubulin and four other unidentified sequences (RBA3, RBA4, RBB3 and RBB5) were found to be upregulated in the hypothyroid brain, whereas another (RBE7) was downregulated. Binding sites for the T3 receptor (T3R/c‐erbA) were identified in the isolated clones by gel‐shift and footprinting assays. Sites in the NCAM (in an intron), alpha‐tubulin (in an exon) and RBA4 clones mediated transcriptional regulation by T3 when inserted upstream of a reporter construct. However, no effect of the NCAM clone was found when located downstream of another reporter gene. Northern blotting and in situ hybridization studies showed a higher expression of NCAM in the brain of postnatal hypothyroid rats. Since NCAM is an important morphoregulatory molecule, abnormal NCAM expression is likely to contribute to the alterations present in the brain of thyroid‐deficient humans and experimental animals.

show abstract

“…wt form of secreted NCAM [25], The main ligands of NCAM, apart from itself, are heparan sulphate [26], type I collagen [27] and the brain proteins spectrin and fodrin [28]. In vitro the expression of NCAM is induced by transforming growth factor-beta (TGF-/3) and fibroblast-conditioned medium [29] and inhibited by transfection with N-myc under a strong promotor [30], A striking increase in NCAM expression has been observed in the myocytes of hypothyroid animals [31].…”

Section: Discussionmentioning

confidence: 99%

Characterization of neural cell adhesion molecule (NCAM) expression in thyroid follicular cells: Induction by cytokines and over expression in autoimmune glands

Vargas

Tolosa

Sospedra

et al. 1994

Clinical and Experimental Immunology

View full text Add to dashboard Cite

SUMMARYNCAM (CD56) is a cell surface glyeoprotein of the immunoglobulin superfamily expressed on neuroendocrine and natural killer (NK) eells which has considerable molecular heterogeneity due to differential splicing and post-translational modifications. NCAM has been detected in the thyroid foHicuIar cells (thyrocytes) immunohistoiogically. We report here the molecular form, the modulation by cytokines and the levels of expression in thyroid pathology. By using a panel of MoAbs to NCAM on Western blots from thyrocyte extract we have determined that these cells express the 140-and I80-kD forms of NCAM, Exposure of primary cultures of thyrocytes to interferon-gamma (IFN-7), and even more, to the combination of IFN-7 plus tumour necrosis factor-alpha (TNF-a) induced a clear increase in the expression of NCAM as assessed by FACS analysis. NCAM expression in thyrocytes was assessed by immunofluorescence in 59 surgical specimens of thyroid glands, atid was found increased in 11/17 (64%) of Graves', in 5/25 (20%) of multinodular goitre (MNG) and in occasional adenoma glands. No correlation was found with the expression of HLA class I. class II or the degree of lymphocytic infiltration scored in adjacent sections, but it was often seen in areas infiltrated by macrophagcs. In conclusion, NCAM is an adhesion molecule whose expression is clearly increased in thyrocytes in autoimmune glands, probably as a consequence of exposure to cytokines locally released. Since one of the forms of NCAM expressed by thyrocytes has the capability to generate intracellular signal it may play a role in normal thyroid function. In addition, NCAM may facilitate the recognition of Ihyrocytes by lymphocytes, particularly by NK CD56* lymphocytes.

show abstract

Thyroid hormones regulate expression of the neural cell adhesion molecule in adult skeletal muscle

Cited by 23 publications

References 19 publications

Thyroid hormone regulation of myosin heavy chain isoform composition in young and old rats, with special reference to IIX myosin

Thyroid hormone regulation of myosin heavy chain isoform composition in young and old rats, with special reference to IIX myosin

Thyroid hormone-dependent transcriptional repression of neural cell adhesion molecule during brain maturation.

Characterization of neural cell adhesion molecule (NCAM) expression in thyroid follicular cells: Induction by cytokines and over expression in autoimmune glands

Contact Info

Product

Resources

About