Maternal thyroid status regulates the expression of neuronal and astrocytic cytoskeletal proteins in the fetal brain
| Autor: | AK Sinha, A.J. Leonard, Roger Ekins, Ian M. Evans, D.C. Sampson, M. R. Pickard |
|---|---|
| Rok vydání: | 2000 |
| Předmět: |
medicine.medical_specialty
Neurofilament Endocrinology Diabetes and Metabolism Immunoblotting Central nervous system Thyroid Gland Gestational Age Rats Sprague-Dawley Embryonic and Fetal Development Endocrinology Maternal hypothyroidism Intermediate Filament Proteins Internexin Neurofilament Proteins Pregnancy Internal medicine Glial Fibrillary Acidic Protein medicine Animals Vimentin Brain Chemistry Neurons Analysis of Variance Fetus Glial fibrillary acidic protein biology Embryogenesis Brain medicine.disease Rats Cytoskeletal Proteins medicine.anatomical_structure Astrocytes embryonic structures Linear Models Thyroidectomy biology.protein Pregnancy Animal Neuroglia Female Carrier Proteins |
| Zdroj: | Journal of Endocrinology. 167:439-445 |
| ISSN: | 1479-6805 0022-0795 |
| Popis: | Maternal thyroid hormone (TH) crosses the placenta and is postulated to regulate fetal brain development. However, TH-dependent stages of fetal brain development remain to be characterised. We have therefore compared the levels of several neuronal and glial cytoskeletal proteins in fetal brains from normal (N) and partially thyroidectomised (TX) rat dams by immunoblotting. Pregnancies were studied both before and after the onset of fetal TH secretion, which occurs at 17.5 days gestation (dg) in the rat. Maternal hypothyroidism disrupted fetal growth, so that fetal body and brain weights were reduced near term. Vimentin expression was unaffected, however, indicating normal acquisition of neuronal and glial precursor cells. Fetal brain levels of glial fibrillary acidic protein (GFAP) were reduced at 21 dg, suggesting delayed astrocytic differentiation, although regression analysis demonstrated appropriate GFAP levels for brain weight. Levels of alpha-internexin, the earliest neurofilament protein expressed in fetal brain were reduced at 16 dg in TX dams, but increased at 21 dg. The ontogeny of neurofilament-L was also perturbed in these pregnancies, with deficient levels apparent at both 16 and 21 dg. These effects on neuronal cytoskeletal proteins were unrelated to fetal brain growth retardation. These findings confirm that maternal hypothyroidism disrupts early fetal brain development. Early disturbances in neuronal differentiation are not corrected by the onset of fetal TH secretion. Such disturbances may contribute to the neurological damage observed in children born to hypothyroxinaemic mothers. |
| Databáze: | OpenAIRE |
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