Regulation of phosphatidylcholine synthesis in maturing type II cells: increased mRNA stability of CTP:phosphocholine cytidylyltransferase
| Autor: | Maciej Kuliszewski, Martin Post, Wen-Su Lee, Martina Hogan |
|---|---|
| Rok vydání: | 1996 |
| Předmět: |
Male
medicine.medical_specialty Transcription Genetic Cytidylyltransferase Gestational Age Biology Biochemistry Dexamethasone Gene Expression Regulation Enzymologic Choline-phosphate cytidylyltransferase Embryonic and Fetal Development chemistry.chemical_compound Cytosol Fetus Pregnancy Microsomes Internal medicine medicine Animals Choline-Phosphate Cytidylyltransferase RNA Messenger RNA Processing Post-Transcriptional Rats Wistar Lung Molecular Biology Phosphocholine Regulation of gene expression Messenger RNA Developmental induction Cell Biology Nucleotidyltransferases Rats Endocrinology chemistry Phosphatidylcholines Female Glucocorticoid Research Article medicine.drug |
| Zdroj: | Biochemical Journal. 314:799-803 |
| ISSN: | 1470-8728 0264-6021 |
| DOI: | 10.1042/bj3140799 |
| Popis: | Pulmonary surfactant phosphatidylcholine synthesis increases in fetal lung type II cells with advancing gestation. This increase is accompanied by an increase in gene and protein expression of CTP:phosphocholine cytidylyltransferase (CT; EC 2.7.7.15), which catalyses a regulatory step in de novo phosphatidylcholine synthesis by fetal type II cells. In the present study we investigated the role of transcriptional and post-transcriptional mechanisms in the developmental induction of CT mRNA in maturing type II cells. We found that CT mRNA increased 2-fold from days 18 to 21 of fetal rat gestation (term 22 d). This increase in CT mRNA was not accompanied by a developmental increase in CT gene transcription. However, CT mRNA was more stable on day 21 (t½ 48 h) compared with that on day 18 (t½ 17 h). Glucocorticoids have been shown to enhance surfactant phosphatidylcholine synthesis in fetal type II cells. Therefore we also examined the effect of maternal glucocorticoid administration to pregnant rats at 19 d of gestation on CT mRNA expression in fetal type II cells isolated 24 h later. Glucocorticoid treatment did not increase type II cell CT mRNA. As reported previously, however, glucocorticoids increased CT activity in the microsomal membrane fraction of fetal type II cells, whereas no differences in cytosolic CT activity were observed. We conclude that the developmental increase in CT mRNA in fetal type II cells is due to a decreased breakdown of the CT transcript and that glucocorticoids regulate fetal type II cell CT activity at a post-translational level. |
| Databáze: | OpenAIRE |
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