Thyroid hormone induces protein secretion and morphological changes in astroglial cells with an increase in expression of glial fibrillary acidic protein

Lima, Flávia Farias; Trentin, Andréa Gonçalves; Rosenthal, Doris; Chagas, Carlos; Moura‐Neto, Vivaldo

doi:10.1677/joe.0.1540167

Cited by 65 publications

(56 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Similar to other neural cells (Walter, 1996;Baas et al, 1997;Lima et al, 1997), purified ameboid microglial cells respond to T3 exposure by increased extension of cell processes, an important step in their acquisition of a ramified phenotype. As for the effect on cell survival, it may be hypothesized that increased or decreased levels of T3 reaching microglial cells contribute to augment or reduce microglial process formation in hyperthyroid and hypothyroid rats, respectively.…”

Section: Pathways For Thyroid Hormone Influences On Microglia: Assessmentioning

confidence: 98%

“…These compounds favor basic processes of neurogenesis, including precursor cell proliferation, neuronal migration, dendritic and axonal growth, myelination, and synaptogenesis (Legrand, 1983;Porterfield and Hendrich, 1993;Bernal and Nunez, 1995). Thyroid hormone also acts as a promoter of astroglial and oligodendroglial differentiation and modulates proliferation of macroglial cells, depending on their stage of maturation and their localization in the brain (Rami and Rabié, 1988;Faivre-Sarrailh et al, 1991;Trentin et al, 1995;Lima et al, 1997Lima et al, , 1998Rodríguez-Peña, 1999).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Regulation of Microglial Development: A Novel Role for Thyroid Hormone

et al. 2001

View full text Add to dashboard Cite

The postnatal development of rat microglia is marked by an important increase in the number of microglial cells and the growth of their ramified processes. We studied the role of thyroid hormone in microglial development. The distribution and morphology of microglial cells stained with isolectin B4 or monoclonal antibody ED1 were analyzed in cortical and subcortical forebrain regions of developing rats rendered hypothyroid by prenatal and postnatal treatment with methyl-thiouracil. Microglial processes were markedly less abundant in hypothyroid pups than in age-matched normal animals, from postnatal day 4 up to the end of the third postnatal week of life. A delay in process extension and a decrease in the density of microglial cell bodies, as shown by cell counts in the developing cingulate cortex of normal and hypothyroid animals, were responsible for these differences. Conversely, neonatal rat hyperthyroidism, induced by daily injections of 3,5,3Ј-triiodothyronine (T3), accelerated the extension of microglial processes and increased the density of cortical microglial cell bodies above physiological levels during the first postnatal week of life.Reverse transcription-PCR and immunological analyses indicated that cultured cortical ameboid microglial cells expressed the ␣1 and ␤1 isoforms of nuclear thyroid hormone receptors. Consistent with the trophic and morphogenetic effects of thyroid hormone observed in situ, T3 favored the survival of cultured purified microglial cells and the growth of their processes. These results demonstrate that thyroid hormone promotes the growth and morphological differentiation of microglia during development.

show abstract

Section: Pathways For Thyroid Hormone Influences On Microglia: Assessmentioning

confidence: 98%

mentioning

confidence: 99%

Regulation of Microglial Development: A Novel Role for Thyroid Hormone

et al. 2001

View full text Add to dashboard Cite

show abstract

“…This effect was accompanied by reorganization of GFAP filaments that were spread in the cytoplasm of astrocytes and became organized around the cell nucleus after T 3 treatment (7). In those experiments, we observed that total GFAP expression was not changed (8). Thus, thyroid hormone seems to control many aspects of astrocyte differentiation.…”

Section: T 3 Regulates Protein Expression In C6 Cellsmentioning

confidence: 83%

“…The growth factors secreted by cerebral hemisphere astrocytes promote morphological differentiation in cells derived from cerebral hemispheres of normal and hypothyroid newborn rats. In contrast, the growth factors secreted by cerebellar astrocytes induce proliferation in astrocytes from normal neonatal cerebellum, accompanied by reorganization of glial fibrillary acidic protein (GFAP) filaments without changes in total GFAP amount (6)(7)(8).…”

mentioning

confidence: 99%

Thyroid hormone regulates protein expression in C6 glioma cells

Trentin¹,

Alvarez-Silva

1998

Braz J Med Biol Res

View full text Add to dashboard Cite

Thyroid hormone (T 3 ) is essential to normal brain development. Previously, we have shown that T 3 induces cerebellar astrocyte proliferation. This effect is accompanied by alteration in glial fibrillary acidic protein (GFAP) and fibronectin organization. In the present study, we report that the C6 glioma cell line, which expresses GFAP and is classified as an undifferentiated astrocytic cell type, is a target for T 3 action. The C6 monolayers were treated with 50 nM T 3 for 3 days, after which the cells were maintained for 2 days without medium changes. In C6 cells, T 3 induced the expression of proteins of 107, 73 and 62 kDa. The hormone also up-regulated protein bands of 100 (+50%), 37 (+50%) and 25.5 kDa (+50%) and down-regulated proteins of 94 (-100%), 86.5 (-100%), 68 (-100%), 60 (-100%), 54 (-33%), 51 (-33%) and 43.5 kDa (-33%). We suggest, on the basis of molecular mass, that the 54-, 51-and 43.5-kDa proteins could be the cytoskeletal proteins vimentin, GFAP and actin, respectively. The down-regulation of these proteins may be involved in the effects of thyroid hormone on C6 differentiation.

show abstract

“…Moreover, T3 can induce GFAP synthesis and astrocyte differentiation (Lima et al 1997). Oestradiol also promotes differentiation of glial cells with a redistribution of GFAP in hypothalamic astrocytes (Torres-Aleman et al 1992, Mong & Blutstein 2006.…”

Section: Discussionmentioning

confidence: 99%

Differential effects of GH and GH-releasing peptide-6 on astrocytes

Baquedano¹,

Chowen²,

Argente³

et al. 2013

Journal of Endocrinology

View full text Add to dashboard Cite

GH and GH secretagogues (GHSs) are involved in many cellular activities such as stimulation of mitosis, proliferation and differentiation. As astrocytes are involved in developmental and protective functions, our aim was to analyse the effects of GH and GH-releasing hexapeptide on astrocyte proliferation and differentiation in the hypothalamus and hippocampus. Treatment of adult male Wistar rats with GH (i.v., 100 mg/day) for 1 week increased the levels of glial fibrillary acidic protein (GFAP) and decreased the levels of vimentin in the hypothalamus and hippocampus. These changes were not accompanied by increased proliferation. By contrast, GH-releasing hexapeptide (i.v., 150 mg/day) did not affect GFAP levels but increased proliferation in the areas studied. To further study the intracellular mechanisms involved in these effects, we treated C6 astrocytoma cells with GH or GH-releasing hexapeptide and the phosphatidylinositol 3 0 -kinase (PI3K) inhibitor, LY294002, and observed that the presence of this inhibitor reverted the increase in GFAP levels induced by GH and the proliferation induced by GH-releasing hexapeptide. We conclude that although GH-releasing hexapeptide is a GHS, it may exert GH-independent effects centrally on astrocytes when administered i.v., although the effects of both substances appear to be mediated by the PI3K/Akt pathway.

show abstract

Thyroid hormone induces protein secretion and morphological changes in astroglial cells with an increase in expression of glial fibrillary acidic protein

Cited by 65 publications

References 18 publications

Regulation of Microglial Development: A Novel Role for Thyroid Hormone

Regulation of Microglial Development: A Novel Role for Thyroid Hormone

Thyroid hormone regulates protein expression in C6 glioma cells

Differential effects of GH and GH-releasing peptide-6 on astrocytes

Contact Info

Product

Resources

About