RGD Reference Report - Proteomic characterization of early changes induced by triiodothyronine in rat liver. - Rat Genome Database
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Proteomic characterization of early changes induced by triiodothyronine in rat liver.

Authors: Severino, V  Locker, J  Ledda-Columbano, GM  Columbano, A  Parente, A  Chambery, A 
Citation: Severino V, etal., J Proteome Res. 2011 Jul 1;10(7):3212-24. Epub 2011 Jun 1.
RGD ID: 5147909
Pubmed: (View Article at PubMed) PMID:21563808
DOI: Full-text: DOI:10.1021/pr200244f

High doses of T3 are mitogenic in liver, causing hyperplasia that has numerous differences from the compensatory regeneration induced by partial hepatectomy (PH). T3 binds to the thyroid hormone receptor (TR), which directly regulates transcription, while PH acts indirectly through signal transduction pathways. We therefore carried out a proteomic analysis to compare early effects of the two treatments. Transcriptome analysis by DNA microarray also confirmed the observed proteomic changes, demonstrating that they were caused by transcriptional regulation. Among the differentially expressed proteins, many are directly or indirectly involved in energy metabolism and response to oxidative stress. Several enzymes of lipid metabolism (e.g., Acaa2, Acads, Hadh, and Echs1) were differentially regulated by T3. In addition, altered expression levels of several mitochondrial proteins (e.g., Hspa9, Atp5b, Cps1, Glud1, Aldh2, Ak2, Acads) demonstrated the known increase of mitochondrial biogenesis mediated by T3. The present results provide insights in changes in metabolic balance occurring following T3-stimulation and define a basis for dissecting the molecular pathways of hepatocyte hyperplasia.

Annotation

Gene Ontology Annotations    

Biological Process

Objects Annotated

Genes (Rattus norvegicus)
Ak2  (adenylate kinase 2)
Atp5f1b  (ATP synthase F1 subunit beta)
Hspa9  (heat shock protein family A (Hsp70) member 9)

Objects referenced in this article
0 Atp5f1a ATP synthase F1 subunit alpha All species

Additional Information