scholarly journals Influence of thyroid hormone on the tissue-specific expression of cytochrome c oxidase isoforms during cardiac development

1997 ◽  
Vol 327 (1) ◽  
pp. 155-160 ◽  
Author(s):  
Julia MEEHAN ◽  
John M. KENNEDY
Keyword(s):  
Thyroid Hormone ◽  
Cardiac Development ◽  
Mrna Levels ◽  
Developmentally Regulated ◽  
Specific Expression ◽  
Tissue Specific ◽  
Protein Subunits ◽  
Rat Hearts ◽  
Neonatal Stage ◽  
Developing Rat

In mammals, cytochrome coxidase (COX) is composed of 13 different protein subunits. In the rat, two nuclear-encoded subunits, COX VIa and VIII, exist as tissue-specific isoforms: heart and liver. Using Northern-blot analysis, the levels of transcripts for the heart and liver isoforms of VIa and VIII were examined in developing rat hearts. The liver isoform was found to be the predominant form of subunit VIa and the exclusive form of VIII in the 18-day fetal hearts. The mRNA levels of the heart isoform of both subunits increased dramatically to reach adult levels by 14 days. Although the levels of the VIa- and VIII-liver isoform mRNAs remained stable throughout early development, their levels decreased by 40 and 36% respectively between the 18-day fetal stage and 18-day neonatal stage. Therefore the up-regulation of the heart isoforms and down-regulation of the liver isoforms appear to be regulated in a co-ordinated manner during development. To determine if thyroid hormone influences the expression of these developmentally regulated isoforms, the RNA was also extracted from the hearts of 2-week-old hypothyroid rats. The results showed that the levels of VIII-heart and VIa-liver COX mRNAs were approx. 40% lower in the hypothyroid hearts, while VIII-liver and VIa-heart COX isoform expression remained unchanged. These data demonstrate that the isoforms of COX subunits VIa and VIII are not co-ordinately regulated by changes in thyroid hormone levels. Therefore we conclude that, although thyroid hormone influences the expression of isoforms, it appears to do so via a different mechanism from that which regulates the developmental transition.

scholarly journals Thyroid Hormone Regulates Oligodendrocyte Accumulation in Developing Rat Brain White Matter Tracts

Endocrinology ◽  
2004 ◽  
Vol 145 (11) ◽  
pp. 5013-5020 ◽  
Author(s):  
Christopher M. Schoonover ◽  
Melissa M. Seibel ◽  
Dawn M. Jolson ◽  
Mary Jo Stack ◽  
Rounak J. Rahman ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Rat Brain ◽  
Basic Protein ◽  
Anterior Commissure ◽  
Mrna Levels ◽  
Structural Protein ◽  
Mrna Accumulation ◽  
Brain White Matter ◽  
Perinatal Hypothyroidism ◽  
Developing Rat

Abstract Thyroid hormone (TH) is necessary for normal axonal myelination. Myelin basic protein (MBP) is a structural protein essential for myelin function. In this study, we demonstrate that perinatal hypothyroidism regulates MBP mRNA levels via indirect mechanisms. We observed decreased MBP mRNA accumulation in the hypothyroid rat brain at postnatal (PN) d 10 and 50. Acute TH replacement did not rescue hypothyroid MBP mRNA levels at PN5, 10, or 50. TH is necessary for normal intrahemispheric commissure development including the anterior commissure (AC) and the corpus callosum (CC). We determined that perinatal hypothyroidism decreases AC area and cellularity in the developing rat brain by PN10 and 50. In the developing CC, hypothyroidism initially increases area and cellularity by PN5, but then ultimately decreases area and cellularity by PN50. MBP-expressing oligodendrocytes are a recognized target of TH and are responsible for myelination within intrahemispheric commissures. We found that hypothyroidism reduces the number of mature oligodendrocytes within both the AC and CC. This reduction is noted at PN5, 10, and 50 in the AC and by PN10 and 50 in the CC. Together, these data suggest that TH regulates MBP mRNA levels through indirect mechanisms. These data demonstrate the complex mechanisms whereby TH regulates myelination in the developing brain.

scholarly journals Tissue-specific regulation of the expression of rat kallikrein gene family members by thyroid hormone

1990 ◽  
Vol 267 (3) ◽  
pp. 745-750 ◽  
Author(s):  
J A Clements ◽  
B A Matheson ◽  
J E Funder
Keyword(s):  
Gene Family ◽  
Hormonal Regulation ◽  
Female Rats ◽  
Hormonal Status ◽  
Mrna Levels ◽  
Specific Expression ◽  
Male And Female ◽  
Tissue Specific ◽  
Male And Female Rats ◽  
Specific Regulation

We have altered the thyroid hormonal status of both male and female rats and examined the expression of six functional members of the rat kallikrein gene family (PS, S1, S2, S3, K1 and P1) in the submandibular gland (SMG), kidney, prostate, testis and anterior pituitary gland (AP) of these animals. On Northern-blot analysis with gene-specific oligonucleotide probes, the steady-state mRNA levels of S1, S2, S3, K1 and P1 were all dramatically altered in the SMG of male and female rats treated with propylthiouracil (PTU; 100 mg/litre of drinking water) or thyroxine (T4; 10 micrograms/100 mg body wt.) for 3 weeks. The SMG mRNA levels of these five genes were all lowered (30-90%) in hypothyroid (PTU-treated) male and female rats and elevated (1.4-4-fold, male; 1.5-11-fold, female) in the hyperthyroid (T4-treated) and PTU/T4-treated animals. In contrast, PS (true kallikrein) mRNA levels in the male or female SMG or kidney were essentially unchanged. K1 mRNA levels in the kidney were considerably less responsive to thyroid status than those in the SMG. Changes in S3 and P1 mRNA levels in the prostate were also variable, but essentially unaffected by these treatments. AP PS mRNA levels were also unaffected by changes in thyroid-hormonal status, as were levels of a novel P1-like mRNA in the testis. In summary, these studies demonstrate that the same kallikrein gene family member(s) may be differentially regulated by thyroid hormones in the rat SMG, kidney, prostate and pituitary, and thus further extend the concept of tissue-specific expression and hormonal regulation of the kallikrein gene family in the rat.

Frataxin Shows Developmentally Regulated Tissue-Specific Expression in the Mouse Embryo

1997 ◽  
Vol 4 (2) ◽  
pp. 103-113 ◽  
Author(s):  
Sarn Jiralerspong ◽  
Yanling Liu ◽  
Laura Montermini ◽  
Stefano Stifani ◽  
Massimo Pandolfo
Keyword(s):  
Mouse Embryo ◽  
Developmentally Regulated ◽  
Specific Expression ◽  
Tissue Specific ◽  
Tissue Specific Expression

Cinnamon intake reduces serum T3 level and modulates tissue-specific expression of thyroid hormone receptor and target genes in rats

2015 ◽  
Vol 96 (8) ◽  
pp. 2889-2895 ◽  
Author(s):  
Thaiane G Gaique ◽  
Bruna P Lopes ◽  
Luana L Souza ◽  
Gabriela S M Paula ◽  
Carmen C Pazos-Moura ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Hormone Receptor ◽  
Target Genes ◽  
Thyroid Hormone Receptor ◽  
Specific Expression ◽  
Tissue Specific ◽  
Tissue Specific Expression ◽  
Serum T3

Differential expression of the neurotensin gene in the developing rat and human gastrointestinal tract

1993 ◽  
Vol 265 (3) ◽  
pp. G482-G490 ◽  
Author(s):  
B. M. Evers ◽  
S. Rajaraman ◽  
D. H. Chung ◽  
C. M. Townsend ◽  
X. Wang ◽  
...  
Keyword(s):  
Small Bowel ◽  
Human Colon ◽  
Developmental Expression ◽  
N Gene ◽  
Mrna Levels ◽  
Specific Expression ◽  
Fetal Rat ◽  
Topographical Distribution ◽  
Neuromedin N ◽  
Developing Rat

Neurotensin (NT) is an important hormone regulating gut motility, secretion, and growth. The purpose of this study was to determine the developmental expression of the NT/neuromedin N gene (NT/N) in the gut and pancreas of rats and humans. We found that NT/N expression, initially low in the fetal rat jejunum and ileum, is increased by postnatal day 3. This increase is independent of contact with luminal nutrients as demonstrated by elevated NT/N expression in rat jejunoileal grafts implanted in nude mice. NT/N expression reaches maximal levels in the small bowel by postnatal day 14. After postnatal day 28, NT/N mRNA levels remain constant in the ileum but decrease in the jejunum. Transient NT/N expression is found in the colon of fetal and postnatal rats. Similar to the rat, NT/N expression is low in the human fetal ileum but increases in the adult. In the human colon, NT/N is transiently expressed in the fetus at midgestation but disappears by birth and, similarly, is not apparent in the adult. We conclude the following. 1) The NT/N gene demonstrates a complex pattern of tissue-specific expression; the jejunum and ileum show a similar pattern of expression until the end of the fourth postnatal week, when NT/N levels decrease in the jejunum to assume the distinctive adult topographical distribution with NT/N increasing along the jejunoileal axis. 2) NT/N is transiently expressed in the colon of rats and humans during a developmental stage characterized by morphological and functional similarities to the small bowel; therefore, NT/N may provide a useful endocrine marker to further define the complex differentiation pathway leading to small bowel and colonic phenotypes.

scholarly journals Tissue-specific regulation of thyroid hormone receptor mRNA isoforms and target gene proteins in domestic ducks

2000 ◽  
Vol 165 (3) ◽  
pp. 607-615 ◽  
Author(s):  
CM Bishop ◽  
CJ McCabe ◽  
NJ Gittoes ◽  
PJ Butler ◽  
JA Franklyn
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Body Mass ◽  
Thyroid Hormone Receptor ◽  
Mrna Isoforms ◽  
Specific Expression ◽  
Primary Feather ◽  
Tissue Samples ◽  
Tissue Specific ◽  
Specific Regulation

Skeletal muscles are important target tissues for thyroid hormone action. The present study examines the influence of thyroid status on muscle growth and tissue-specific expression of thyroid receptor (TR) mRNA isoforms in a commercial strain of the domestic duck (Anas platyrhynchos). Four groups (n=5) of 1-week-old ducklings were rendered either hypothyroid by treatment with methimazole (6 mg 100 g(-1) body mass or 12 mg 100 g(-1) body mass), or hyperthyroid by treatment with methimazole (6 mg 100 g(-1) body mass) in combination with thyroid hormones (5 microg thyroxine (T(4)) and tri-iodothyronine (T(3)) 100 g(-1) body mass or 10 microg T(4) and T(3) 100 g(-1) body mass). Serum and tissue samples (cardiac, pectoralis and semimembranosus leg muscle, liver, pituitary and cerebral cortex) were collected from these four groups, and from a group of untreated controls, at 8 weeks of age. Development of duckling morphology was retarded in methimazole-treated birds compared with that in euthyroid controls, as evidenced by differences in skeletal dimensions, primary feather length, and body and muscle masses. Body mass was lower by 18%, and relative masses of cardiac and pectoralis muscles were lower by 28% and 32% respectively. Heterologous oligonucleotides for TR alpha, TR beta 0, TR beta2 and the housekeeping gene beta-actin were derived from chicken sequences. RT-PCR showed that TR alpha mRNA was expressed in all tissues but was not significantly affected by any of the experimental treatments. TR beta 0 mRNA expression was significantly lower in the leg muscles of ducklings treated with 12 mg methimazole 100 g(-1) body mass (0.109+/-0.047 TR:beta-actin ratio, P<0.05) compared with that in euthyroid controls (0.380+/-0.202), but was unaltered in the pectoralis and cardiac muscles. Expression of TR beta 0 mRNA was significantly higher in pectoralis (by 3.5-fold, P<0. 05), cardiac (by 4.2-fold, P=0.003) and leg (by 4.0-fold, P<0.001) muscles of ducklings treated with thyroid hormones compared with those in euthyroid controls (0.098+/-0.019, 0.822+/-0.297 and 0. 38+/-0.202 TR:beta-actin respectively). Only the pituitary gland expressed significant levels of TR beta 2 mRNA.

scholarly journals Histone H2B monoubiquitination regulates heart development via epigenetic control of cilia motility

2019 ◽  
Vol 116 (28) ◽  
pp. 14049-14054 ◽  
Author(s):  
Andrew Robson ◽  
Svetlana Z. Makova ◽  
Syndi Barish ◽  
Samir Zaidi ◽  
Sameet Mehta ◽  
...  
Keyword(s):  
Chromatin Remodeling ◽  
Heart Development ◽  
Loss Of Function ◽  
Developmentally Regulated ◽  
Specific Expression ◽  
Histone H2b ◽  
Tissue Specific ◽  
Heart Looping ◽  
Significant Enrichment ◽  
Gene Ontologies

Genomic analyses of patients with congenital heart disease (CHD) have identified significant contribution from mutations affecting cilia genes and chromatin remodeling genes; however, the mechanism(s) connecting chromatin remodeling to CHD is unknown. Histone H2B monoubiquitination (H2Bub1) is catalyzed by the RNF20 complex consisting of RNF20, RNF40, and UBE2B. Here, we show significant enrichment of loss-of-function mutations affecting H2Bub1 in CHD patients (enrichment 6.01,P= 1.67 × 10−03), some of whom had abnormal laterality associated with ciliary dysfunction. InXenopus, knockdown ofrnf20andrnf40results in abnormal heart looping, defective development of left–right (LR) asymmetry, and impaired cilia motility. Rnf20, Rnf40, and Ube2b affect LR patterning and cilia synergistically. Examination of global H2Bub1 level inXenopusembryos shows that H2Bub1 is developmentally regulated and requires Rnf20. To examine gene-specific H2Bub1, we performed ChIP-seq of mouse ciliated and nonciliated tissues and showed tissue-specific H2Bub1 marks significantly enriched at cilia genes including the transcription factorRfx3. Rnf20 knockdown results in decreased levels ofrfx3mRNA inXenopus, and exogenousrfx3can rescue the Rnf20 depletion phenotype. These data suggest that Rnf20 functions at theRfx3locus regulating cilia motility and cardiac situs and identify H2Bub1 as an upstream transcriptional regulator controlling tissue-specific expression of cilia genes. Our findings mechanistically link the two functional gene ontologies that have been implicated in human CHD: chromatin remodeling and cilia function.

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