Plasma protein regulation by thyroid hormone
| Autor: | Chun-Che Yen, Kai-Hsin Lin, Chung Hsuan Shih, RC Yang, Chuang-Wei Wang, Shen Liang Chen, HY Lee |
|---|---|
| Rok vydání: | 2003 |
| Předmět: |
Transcriptional Activation
Thyroid Hormones medicine.medical_specialty DNA Complementary Transcription Genetic Endocrinology Diabetes and Metabolism Transferrin receptor Biology Prothymosin Alpha Endocrinology Internal medicine Gene expression Tumor Cells Cultured medicine Humans RNA Messenger Northern blot Regulation of gene expression chemistry.chemical_classification Thyroid hormone receptor Dose-Response Relationship Drug Transferrin Blood Proteins Blotting Northern Molecular biology Gene Expression Regulation chemistry Thyroid hormone receptor alpha Triiodothyronine Thyroid Hormone Receptors alpha |
| Zdroj: | Journal of Endocrinology. 179:367-377 |
| ISSN: | 1479-6805 0022-0795 |
| DOI: | 10.1677/joe.0.1790367 |
| Popis: | Thyroid hormones (THs) regulate growth, development, differentiation and metabolic processes by interacting and activating thyroid hormone receptors (TRs). Although much progress has been made in our understanding of the transcriptional regulation of many TR target genes, little is known of the regulation of plasma protein gene expression by TRs. To investigate the role of TRs in plasma protein expression we used human hepatocellular carcinoma cell lines and carried out cDNA microarray analysis. Our results indicate that several plasma proteins including transferrin, prothrombin, angiotensinogen, haptoglobin, alpha-2-HS-glycoprotein alpha and beta chain, complement, lipoproteins and fibrinogen are up-regulated by THs. Furthermore, clusterin, alpha-2-macroglobulin precursor, prothymosin alpha and alpha-fetoprotein were found to be down-regulated by THs.Transferrin, an iron-binding protein expressed in all mammals, and mainly synthesized in the liver, was investigated further. Immunoblot and Northern blot analyses revealed that exposure of HepG2-TRalpha1 sub-lines and HepG2-Neo cells to tri-iodothyronine (T(3)) induced time- and dose-dependent increases in the abundance of transferrin mRNA and protein, with the extent of these effects correlating with the level of expression of TRalpha1. Nuclear run-on experiments indicate that this induction is functioning at the transcriptional level. Moreover, cyclohexamide treatment did not eliminate the induction of transferrin by TH. Thus, our results suggest that the induction of transferrin by TH is direct and may in fact be mediated by an as yet unidentified response element in the promoter region. |
| Databáze: | OpenAIRE |
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