PubMed Health⌕ Search

Biomedical subjects

F C Gomes

Publications and source records attributed to F C Gomes.

13 recordsLinked to original sources
PubMed2001

Cross-talk between neurons and glia: highlights on soluble factors.

The development of the nervous system is guided by a balanced action between intrinsic factors represented by the genetic program and epigenetic factors characterized by cell-cell interactions which neural cells might perform throughout nervous system morphogenesis. Highly relevant among them are neuron-glia interactions. Several soluble factors secreted by either glial or neuronal cells have been implicated in the mutual influence these cells exert on each other. In this review, we will focus our attention on recent advances in the understanding of the role of glial and neuronal trophic factors in nervous system development. We will argue that the functional architecture of the brain depends on an intimate neuron-glia partnership.

Animals↗
PubMed2000

[Diagnosis of cerebellum-pontine angle tumors using artificial intelligence techniques].

We are concerned in this paper with learning classification procedures from known cases. More precisely, we provide a diagnostic model that discriminate between cerebellum-pontine angle (CPA) tumors and otorhinolaryngological (ENT) disorders. Usually, in order to distinguish between CPA tumors and ENT disorders one must perform clinical-neurological examination together with expensive radiological imagery (CT and MRI). The proposed model was obtained through artificial intelligence methods and presented a good accuracy level (88.4%) when tested against new cases, considering only clinical examination without radiological imagery results.

Artificial Intelligence↗
PubMed1999

Cerebellar astrocytes treated by thyroid hormone modulate neuronal proliferation.

Thyroid hormones are important for neurogenesis and gliogenesis during brain development. We have previously demonstrated that triiodothyronine (T3) treatment induced proliferation in primary culture astrocytes derived from the cerebellum of neonatal rats. Conditioned medium obtained from those T3-treated astrocytes (T3CM) mimicked the effect of hormonal treatment on these cells. Because neuron-glia interaction plays an important role in brain development, we tested the ability of such T3-glial CM to influence neuronal physiology. With that aim, neurons from 19-day embryonic cerebella were cultivated for 24 h in the presence of CM obtained from T3-treated cerebellar astrocytes. Interestingly, the cerebellar neuronal population increased by 60-80% in T3CM. Addition of 5 microM forskolin enhanced the responsiveness of cerebellar neurons to astrocytes T3CM, but it did not interfere with neuronal survival in control medium. Conversely, inhibition of adenylate cyclase by its specific inhibitor, SQ22536, reversed the T3CM effect on neurons. These data strongly suggest that cAMP signal transduction pathways might be implicated in such an event. Analysis of bromodeoxyuridil incorporation revealed that the increase in neuron number in T3CM was partially due to neuron proliferation, because the proliferation index was three times higher in T3CM than in control medium. Neutralizing antibody assays demonstrated that T3CM effects on neurons are due, at least in part, to the presence of tumor necrosis factor-beta and epidermal growth factor. Thus, we report here a novel molecular mechanism of action of thyroid hormone on cerebellar neuronal cells: Thyroid hormone induces astrocytes to secrete growth factors that can interfere with neuronal proliferation via a paracrine pathway.

Animals↗
PubMed1999

Neurons induce GFAP gene promoter of cultured astrocytes from transgenic mice.

In order to investigate the influence of neuron-glia interaction on astrocyte differentiation, we used a transgenic mouse bearing part of the gene promoter of the astrocytic maturation marker GFAP linked to the beta-galactosidase (beta-gal) reporter gene. Addition of embryonic cerebral hemisphere (CH) neurons to transgenic CH astrocyte monolayers increased by 50-60% beta-gal positive cell number. Such event was dependent on the brain regional origin of the neurons and was followed by an arrest of astrocytes from the cell cycle and induction of glial differentiation. Time-course assays demonstrated that maximum effect was observed after 24 h of coculture. Addition of conditioned medium (CM) derived from CH neurons also increased beta-gal positive CH astrocytic cell number. However, such CM had no effect on midbrain and cerebellum astroglia. Together, these data suggest that neurons secrete brain region-specific soluble factors which induce GFAP gene promoter, as measured by beta-gal expression, thus suggesting that neuron-glia interaction might induce the astrocytic differentiation program.

Animals↗
PubMed1999

Regulatory roles of microtubule-associated proteins in neuronal morphogenesis. Involvement of the extracellular matrix.

As a result of recent investigations, the cytoskeleton can be viewed as a cytoplasmic system of interconnected filaments with three major integrative levels: self-assembling macromolecules, filamentous polymers, e.g., microtubules, intermediate filaments and actin filaments, and supramolecular structures formed by bundles of these filaments or networks resulting from cross-bridges between these major cytoskeletal polymers. The organization of this biological structure appears to be sensitive to fine spatially and temporally dependent regulatory signals. In differentiating neurons, regulation of cytoskeleton organization is particularly relevant, and the microtubule-associated protein (MAP) tau appears to play roles in the extension of large neuritic processes and axons as well as in the stabilization of microtubular polymers along these processes. Within this context, tau is directly involved in defining neuronal polarity as well as in the generation of neuronal growth cones. There is increasing evidence that elements of the extracellular matrix contribute to the control of cytoskeleton organization in differentiating neurons, and that these regulations could be mediated by changes in MAP activity. In this brief review, we discuss the possible roles of tau in mediating the effects of extracellular matrix components on the internal cytoskeletal arrays and its organization in growing neurons.

Cytoskeletal Proteins↗
PubMed1999

Glial fibrillary acidic protein (GFAP): modulation by growth factors and its implication in astrocyte differentiation.

Intermediate filament (IF) proteins constitute an extremely large multigene family of developmentally and tissue-regulated cytoskeleton proteins abundant in most vertebrate cell types. Astrocyte precursors of the CNS usually express vimentin as the major IF. Astrocyte maturation is followed by a switch between vimentin and glial fibrillary acidic protein (GFAP) expression, with the latter being recognized as an astrocyte maturation marker. Levels of GFAP are regulated under developmental and pathological conditions. Upregulation of GFAP expression is one of the main characteristics of the astrocytic reaction commonly observed after CNS lesion. In this way, studies on GFAP regulation have been shown to be useful to understand not only brain physiology but also neurological disease. Modulators of GFAP expression include several hormones such as thyroid hormone, glucocorticoids and several growth factors such as FGF, CNTF and TGF beta, among others. Studies of the GFAP gene have already identified several putative growth factor binding domains in its promoter region. Data obtained from transgenic and knockout mice have provided new insights into IF protein functions. This review highlights the most recent studies on the regulation of IF function by growth factors and hormones.

Astrocytes↗
PubMed1998

Thyroid hormone action on astroglial cells from distinct brain regions during development.

Astrocytes are target to triiodothyronine (T3) hormone action during rat brain development. In this work, we show that astrocytes from distinct developing brain regions are differently responsive to thyroid hormone. Distinctly from embryonic or newborn cerebral hemisphere and mesencephalic astrocytes, newborn cerebellar and embryonic hippocampal astrocytes do not change their morphology in response of hormone treatment. We also analysed protein synthesis and secretion from these T3-treated astrocytes. The results showed a significant increase in protein synthesis in astrocytes from older brain regions. Maximum effect, however, was observed in cerebral hemisphere astrocytes from newborn rats. The protein secretion effect was also more evident in the cerebral hemisphere as well as in cerebellar astrocytes from newborn rats. In addition, we examined T3 effects on GFAP/vimentin expression by culturing 6-day old cerebellar astrocytes. In this case T3 seems to induce GFAP expression which might be occurring as a first step to astrocyte differentiation.

Animals↗
PubMed1995

Leishmania amazonensis: multidrug resistance in vinblastine-resistant promastigotes is associated with rhodamine 123 efflux, DNA amplification, and RNA overexpression of a Leishmania mdr1 gene.

A vinblastine-resistant Leishmania amazonensis cell line (RV100) which exhibits cross-resistance to the unrelated drug adriamycin, and thus is considered to be multidrug resistant (MDR), was isolated after stepwise selection with increasing concentrations of vinblastine. This phenotype was partially reverted by the calcium channel antagonist verapamil. Drug transport studies using the hydrophobic fluorescent dye rhodamine 123 demonstrated that the MDR cell line has a reduced dye accumulation due to an increased efflux. Furthermore, DNA and RNA hybridization studies demonstrated that a gene (lamdr1), homologous to ldmdr1 and lemdr1, was overexpressed and amplified within 27 kb extrachromosomal DNA circles (V-circles) in these cells. An independent cell line, RA5000, which was selected for resistance to adriamycin and was not cross-resistant to vinblastine, accumulated normal levels of rhodamine 123 and did not contain amplified DNA or overexpressed RNA of mdr-related sequences.

ATP Binding Cassette Transporter, Subfamily B, Mem↗