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Results for “Phenotype modifier”

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At least 721 records · Page 40Linked to original sources

PubMed2000

Effect of thyroid hormone on mtHsp70 expression, mitochondrial import and processing in cardiac muscle.

Mitochondrial heat shock protein 70 (mtHsp70), an important mitochondrial chaperone, is increased in cardiac muscle mitochondria of hyperthyroid rats. To determine the mechanism(s) underlying this increase, we used variations in thyroid status. In Series I, rats were made hyperthyroid by injecting them with 3,3', 5-triiodo-l-thyronine (T(3)) for 5 days, or by treating them with vehicle. In Series II, animals were given 6-n-propyl-2-thiouracil in their drinking water (0.05% w/v) for a period of 32-42 days to make them hypothyroid. During the last 5 days of treatment these animals received injections of either T(3) or vehicle. T(3) treatment resulted in parallel increases in mtHsp70 protein and mRNA levels in a variety of tissues, suggesting transcriptional regulation. However, evidence of tissue-specific post-transcriptional regulation was also apparent. In isolated heart mitochondria, T(3) treatment resulted in a 1.8-fold increase in mtHsp70. This was due to the 1. 6-fold greater import of mtHsp70 into mitochondria in T(3), compared with hypothyroid animals, and it could not be attributed to an altered rate of intramitochondrial mtHsp70 degradation. The rate of processing of mtHsp70 to its mature form, reflecting mitochondrial processing peptidase activity, was unaffected by T(3), but was more rapid than mtHsp70 import. These data indicate a novel mechanism by which T(3) modifies the mitochondrial phenotype via the adaptations in the protein import pathway.

Animals↗

PubMed2005

Do substance P and the NK1 receptor have a role in depression and anxiety?

Research on Substance P (SP) has, until recently, focused on its role in pain and inflammation. However, a report that NK(1) receptor antagonists have utility in the treatment of depression has stimulated research into the function of SP and the NK(1)receptor in anxiety and depression. The distribution of SP and the NK(1) receptor in brain areas implicated in anxiety and depression is initially reviewed. This is followed by evaluation of the preclinical data obtained for SP and NK(1) receptor antagonists in behavioral models of depression as well as the phenotype of genetically modified animals lacking the genes encoding for the NK(1) receptor or for SP. The weight of the evidence supports antidepressant and anxiolytic activity of NK(1) receptor antagonists. However, many of the studies do not control for nonspecific effects of the compounds, and when enantiomers that lack activity at the NK(1) receptor are included, the results, in some cases, suggest that blockade of NK(1) receptors does not account for the observed behavioral activity. Finally, clinical studies in depressed patients assessing SP levels in plasma and cerebrospinal fluid as well as the effect of NK(1) receptor antagonists are reviewed. The clinical studies are a mixture of positive, failed and negative studies on the antidepressant activity of NK(1) receptor antagonists, not unlike the early clinical results obtained with selective serotonin reuptake inhibitors.

Amygdala↗

PubMed2004

The role of cytosolic phospholipase A(2) in insulin secretion.

Cytosolic phospholipase A(2) (cPLA(2)) comprises a widely expressed family of enzymes, some members of which have the properties required of signal transduction elements in electrically excitable cells. Thus, alpha- and beta-isoforms of cPLA(2) are activated by the increases in intracellular Ca(2+) concentration ([Ca(2+)](i)) achieved in depolarized cells. Activation is associated with a redistribution of the enzyme within the cell; activation of cPLA(2) generates arachidonic acid (AA), a biologically active unsaturated fatty acid that can be further metabolized to generate a plethora of biologically active molecules. Studies using relatively nonselective pharmacological inhibitors have implicated cPLA(2) in insulin secretory responses to stimuli that elevate beta-cell [Ca(2+)](i); therefore, we have investigated the role of cPLA(2) in beta-cell function by generating beta-cell lines that under- or overexpress the alpha-isoform of cPLA(2). The functional phenotype of the modified cells was assessed by observation of cellular ultrastructure, by measuring insulin gene expression and insulin protein content, and by measuring the effects of insulin secretagogues on cPLA(2) distribution, on changes in [Ca(2+)](i), and on the rate and pattern of insulin secretion. Our results suggest that cPLA(2) is not required for the initiation of insulin secretion from beta-cells, but that it plays an important role in the maintenance of beta-cell insulin stores. Our data also demonstrate that excessive production of, or exposure to, AA is deleterious to normal beta-cell secretory function through metabolic dysfunction.

Animals↗

PubMed1988

Effects of matrix proteins on rabbit corneal epithelial cell adhesion and migration.

Extracellular matrix and basement membrane proteins are important in promoting the adhesion and migration of various cell types. Laminin and type IV collagen are found in basement membranes throughout the body while fibronectin is found associated with some basal lamina, in loose connective tissue, and in all body fluids. In the current study fibronectin, laminin, and type IV collagen were assessed to determine their effect on the adhesion and migration of dissociated rabbit epithelial cells. In a kinetic analysis fibronectin was found to be the most effective of the three proteins in promoting cell adhesion. Cell adhesion promoted by fibronectin could be modulated by an arg-gly-asp-ser (RGDS) peptide, a sequence which is found within the fibronectin molecule. In dose-response experiments type IV collagen effectively promoted cell adhesion at concentrations as low as 4 x 10(-16) moles per well in 96 well tissue culture plates. Type IV collagen was the most effective protein tested in promoting chemotactic and haptotactic migration. These proteins, proteolytic fragments, and peptides derived from them, could prove useful as therapeutic agents, modifying corneal epithelial phenotypic behavior in wound healing, corneal transplantation and following ocular surgery or trauma.

Animals↗

PubMed1998

Cytokines and cancer.

The relationships between cytokines and cancer are multiple and bidirectional. On the one hand, cytokines may directly influence carcinogenesis and metastasis by modifying the tumor phenotype. On the other hand, during tumor progression, modifications of the cytokine expression in the tumor environment may be induced by the tumor cells, leading to a state of immunosuppression reflected by low cytokine expression in tumor stroma. Cytokines also play a role by stimulating the host immune system to generate anti-tumor specific responses. Finally, the use of cytokines as anti-tumor agents has led to objective clinical responses in about 15-25% of patients with metastatic melanoma or renal cell carcinoma, which presents the basis for the development of promising immunotherapeutic approaches for cancer therapy.

Animals↗

PubMed1996

All-trans retinoic acid (ATRA) and the regulation of adhesion molecules in acute myeloid leukemia.

A review of recent information on the expression and the ATRA-driven modulation of cell surface adhesion molecules of acute myelogenous leukemia blast cells is presented. Cytofluorometric studies on fresh blast cells have demonstrated that CD11a, CD11b CD11c, CD15, CD45RO and CD54 expression is significantly lower in acute promyelocytic leukemia (APL) than is acute myeloid leukemia of other subtypes (AML). In vitro treatment with ATRA dramatically modifies the adhesion phenotype of APL blast cells, promoting a consistently striking up-regulation of CD11b, CD11c, CD15, CD65, CD54, and CD38. Which is in general, poorly demonstrable in AML. The behaviour of CD15s is variable and fully independent from CD15 and CD65 in induction experiments, suggesting a differential enzyme regulation within the selectin ligand system. ATRA is capable, in both APL and AML, of producing a switch from the high- (RA) to the low- (RO) molecular weight isoform of CD54, Moreover, treatment with this retinoid exerts a negative regulation of the membrane expression of CD49e, CD58 and CD11a in APL as well as in AML. Of particular interest is the fact that the negative effect on CD1 1a expression generates an asynchronous phenotype in APL (CD11a-, CD11b+, CD15+), undetectable on normal maturing myeloid cells. In the last part of this review the possible implications of adhesion molecule modulation in the pathogenesis of ATRA syndrome are discussed.

Acute Disease↗

PubMed2005

Delivery of TAT/PTD-fused proteins/peptides to islets via pancreatic duct.

Delivering cytoprotective proteins/peptides into pancreata prior to islet isolation through protein transduction (PT) is a novel strategy to enhance the yield of viable transplantable islets. Previous work has shown that the protein transduction domain PTD-5 efficiently transduced islets via the pancreatic duct. TAT/PTD is a well-characterized PTD with the capability to cross even the hemato-encephalic barrier. In this study, we investigated the utilization of the 11-aa TAT protein transduction domain (TAT/PTD) to deliver peptides or proteins of different sizes ranging from 1.2 to 120 kDa, as the TAT/PTD and TAT/PTD-BH4 peptide, or the TAT/PTD-beta-galactosidase fusion protein, into islets through the pancreatic duct. Using flow cytometry analysis we found that TAT/PTD derivatives transduced practically 100% of the islet cell population. Moreover, confocal laser scanning microscopy in live, nonfixed islets confirmed these results assessing transduction of TAT/PTD molecules into intact nondisaggregated islets. TAT-beta-galactosidase peptide conjugated to FITC was not compartment selective, as both cytoplasmic and nucleic cellular compartments were positively stained. Furthermore, TAT-beta-galactosidase peptide delivery was highly effective, as even cells located in the inner core region of the islets were transduced. Finally, transduced TAT-beta-galactosidase fusion protein was biologically active after islet isolation and manipulation, and islet insulin secretion capability was not compromised by peptide transduction. These findings suggest that the transduction of chimeric TAT/PTD proteins can represent an efficient tool of molecular delivery independent of the size, to enhance or modify a specific phenotype at the nuclei or cytoplasmic level.

Animals↗

PubMed1999

Analysis of 14 CAG repeat-containing genes in schizophrenia.

Recently, it has been suggested that trinucleotide repeat-containing genes may be involved in the etiology of schizophrenia. This study was aimed at investigating putative associations between allelic variants or expansions of CAG repeat-containing genes (CAGrCG) and schizophrenia or its variability with respect to responsiveness to conventional neuroleptics. CAG repeat allelic variants of 14 expressed sequences were compared among three groups of subjects: neuroleptic-responder (R; n = 43) and neuroleptic-nonresponder (NR; n = 63) schizophrenic patients, and a control group (C; n = 122). No CAG expansions, in the range of those observed in neurodegenerative diseases, were identified in these 14 expressed sequences. The sizes of CAG repeat for the hGT1 gene were marginally different among the three groups of subjects (Kruskal-Wallis H (2, 456) = 10.48, Bonferroni corrected P = 0.047). Comparisons among the different groups indicated that neuroleptic responders have shorter alleles compared to controls (Mann-Whitney adjusted Z = -3.23, P = 0.0012). NR patients were not different from controls. These preliminary results suggest that the hGT1 gene, or a gene in its vicinity, may be involved in the etiology of schizophrenia or in modifying the disease phenotype with regard to outcome and/or neuroleptic responsiveness. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 88:694-699, 1999.

Adolescent↗

PubMed2000

[New approaches to the treatment of patients with idiopathic mitral valve prolapse].

AIM: To assess efficiency of magnerot, magnesium orotate, in patients with idiopathic mitral prolapse (IMP). MATERIAL AND METHODS: 84 patients with IMP were randomized to the study group (43 patients) and control group (41 patients). Patients of the study group received magnerot tablets (Germany) containing 500 mg of magnesium orotate (daily dose 3000 mg) for 6 months. The examination performed before the treatment and 6 months after it included: modified clinical and phenotypic records, echocardiography, 24-h ECG and AP monitoring, spectral analysis of cardiac rhythm variability, evaluation of quality of life according to Visual Analog Scale and Disability Scale and of treatment results according to Clinical Global Impression scales, measurements of magnesium in the hair by plasmic nuclear emission spectrometry, histological and histochemical skin tests. RESULTS: IMP patients appeared to suffer from magnesium deficiency which is responsible for many symptoms in mitral prolapse. 6-month therapy with magnerot completely or partially reduced the symptoms in more than half the patients. Positive changes were registered primarily in clinicofunctional manifestations. Morphological changes in the skin correlating with the disease severity alleviated. CONCLUSION: Good objective and subjective response to magnerot 6-month therapy (3000 mg/day) is demonstrated.

Adult↗

PubMed2003

Oligodendrogliomas result from the expression of an activated mutant epidermal growth factor receptor in a RAS transgenic mouse astrocytoma model.

A significant proportion of human malignant gliomas exhibit amplification, overexpression, or mutations of the epidermal growth factor receptor (EGFR). To define the functional role(s) of the EGFR in the pathogenesis of gliomas, we established transgenic mice that express both wild-type (wt) and mutant (EGFRvIII) EGFR molecules using the human glial fibrillary acidic protein (GFAP) promoter. Both GFAP-EGFR(wt) and GFAP-EGFRvIII transgenic mice demonstrated increased numbers of astrocytes compared with control littermates, however, developed normally without formation of gliomas. To determine whether EGFR overexpression could modify the tumor phenotype in our previously reported GFAP-V(12)Ha-ras transgenic mouse astrocytoma model, mice expressing both activated RAS and EGFR were developed. GFAP-V(12)Ha-ras;GFAP-EGFRvIII, but not GFAP-V(12)Ha-ras;GFAP-EGFR(wt) double transgenic mice, had decreased survival with fifty percent of the mice dead at 2-4 weeks from gliomas, compared with 12-16 weeks for the GFAP-V(12)Ha-ras mice. Furthermore, GFAP-V(12)Ha-ras;GFAP-EGFRvIII mice developed oligodendrogliomas and mixed oligoastrocytoma tumors, instead of the fibrillary astrocytomas observed in GFAP-V(12)Ha-ras mice. In addition to yielding a spontaneous model of infiltrating oligodendroglioma, this study demonstrates that astrocyte-specific expression of EGFRvIII alone is insufficient for gliomagenesis but rather contributes to glioma progression in the context of existing predisposing genetic changes.

Animals↗

PubMed2003

Evaluation of alternative reporter genes for the yeast two-hybrid system.

The yeast two-hybrid system is a powerful tool for screening protein-protein interactions and has also been used for large-scale studies. We evaluated two protein-coding sequences as reporter genes for the yeast two-hybrid system, to determine if it was suitable as an alternative screening strategy. Aspergillus awamori glucoamylase activity results in clear haloes around colonies producing this enzyme after growth on starch plates and staining with iodine vapors. However, transcription activation by Gal4 on Gal-regulated promoters was insufficient for this type of phenotypic visualization. A modified gene of Aequoria victoria enhanced green fluorescent protein (EGFP) was tested to determine its suitability for interaction screenings with flow cytometry. When the EGFP reporter gene system was incorporated into the cells, Gal4 transcriptional activation produced sufficient fluorescence for detection with the flow cytometer, especially when there were strong interactions.

Base Sequence↗

PubMed2006

[Nucleotide sequence variants of the glucocorticoid receptor gene and their significance in determining glucocorticoid sensitivity].

Nucleotide sequence variants of the glucocorticoid receptor gene and their significance in determining glucocorticoid sensitivity. The physiologic response and sensitivity to glucocorticoids may significantly differ among species, individuals, tissues and cell types. The variability of the effect of endogenous and exogenous glucocorticoids is largely determined by genetic components, of which the authors review the knowledge on the glucocorticoid receptor gene. The authors describe the genomic and non-genomic pathways of receptor function, the significance of isoforms produced during receptor protein formation, the pathomechanism of glucocorticoid resistance syndrome and the results of clinical investigations related to receptor gene polymorphisms. Through subtle alteration of receptor function, the gene polymorphisms may increase or diminish sensitivity to glucocorticoids and may play a role in the pathogenesis of metabolic disorders. In their own studies the authors found, that the N363S polymorphism, which increases glucocorticoid sensitivity, may play a role in the pathogenesis of bilateral adrenal adenomas, it may modify the clinical phenotype of patients with congenital adrenal hyperplasia, and may have an impact on steroid-induced ocular hypertension. It is presumed that further research in other diseases will continue to complete our knowledge on the pathophysiology of glucocorticoid receptor gene polymorphisms.

Adenoma↗

PubMed1990

Differential production of IL-2 and IL-4 mRNA in vivo after primary sensitization.

The study of lymphokines has been almost entirely conducted by utilizing in vitro assay systems, long term cell lines, and clones. Thus, little information is available concerning the production of lymphokines/cytokines in vivo after specific antigenic stimulation. In order to address this limitation, we have modified the mRNA phenotyping system to allow for the quantitation of lymphokine mRNA after antigenic stimulation in vivo. We report here the production of both IL-2 and IL-4 mRNA in vivo after primary sensitization with picryl chloride. However, the time course of IL-2 and IL-4 mRNA production is discordant. The majority of IL-2 mRNA expression occurs from 1 to 3 days after antigenic exposure, whereas IL-4 mRNA expression occurs mainly from day 3 through day 5. Thus, the production in vivo of these two lymphokine mRNA after sensitization with picryl chloride appears to occur as a "cascade." These results 1) demonstrate that IL-4 mRNA is induced during a primary immune response in vivo and 2) raise the possibility that the generation of an immune response in vivo may involve a specific sequential production of certain lymphokines.

Animals↗

PubMed1990

DNA damage induced by a new 2-chloroethyl nitrosourea on malignant melanoma cells.

Different biological aspects of a novel 2-chloroethyl nitrosourea derived from cysteamine, N'-(2-chloroethyl)-N-[2-(methylsulfinyl)ethyl]-N'- nitrosourea (CMSOEN2), were studied. Drug-induced cytotoxic effects, uptake kinetics, DNA damage, and O6-alkylguanine-DNA alkyltransferase activity were determined in 3 melanoma cell lines: the murine B16 and 2 human metastatic-derived cell lines (M4 Beu and M3 Dau). We found that radioactivity uptake and incorporation in acido-precipitable material was inversely proportional to cell drug viability. The highly CMSOEN2-sensitive B16 line showed the lowest total radioactivity uptake. In fact, among the melanoma cell parameters studied, 3 of them were well correlated: (a) cytotoxicity as reflected by the colony-forming assay; (b) DNA cross-link frequency estimated by the alkaline elution technique; and (c) O6-alkylguanine-DNA alkyltransferase activity (Mer phenotype), defined as the ability of cell extracts to remove O6-methylguanine from N-methyl-N-nitrosourea-alkylated DNA. The 2 human cell lines (M4 Beu and M3 Dau), the most resistant to the cytostatic drug effects, showed little or no ability to form DNA lethal cross-links. These results correspond to the higher O6-alkylguanine-DNA alkyltransferase activity found in human-derived cell lines compared with that present in murine B16 cell lines. This study confirms that the cell content in this repair DNA protein is certainly one of the important factors implicated in the variability of response to 2-chloroethyl nitrosourea treatment observed in a number of established malignant cell lines. It has been shown that pretreatment of derived cell lines with methylating agents (N-methyl-N-nitrosourea, N-methyl-N'-nitro-N-nitrosoguanidine) or O6-methylguanine used as a free base, increased cytotoxic effects of this class of anticancer agents, likely by saturating receptor sites (sulfhydryl groups) of this specific DNA repair enzyme. Nevertheless, in preliminary Phase I and II clinical trials, 2 patients who had been treated with multiple chemotherapies including alkylating agents [1-(2-chloroethyl)-3- cyclohexyl-1-nitrosourea, 5-(3,3-dimethyl-1-triazeno)-imidazole-4-carboxamide, platinum derivatives], presented complete or partial remission after CMSOEN2 treatment. Our results raise the question of the exact relation between the Mer phenotype determined in derived murine or human cultured cells and that directly observed on surgically excised tumors in cancer patients. The original Mer phenotype could be modified by cell culture conditions since it has been shown that O6-alkylguanine-DNA alkyltransferase activity is widely distributed between normal and tumoral tissues without any real difference.

Antineoplastic Agents↗

PubMed1989

[Clinical aspects, epidemiologic progression of fetal alcoholism: a current daily problem].

Foetal and neonatal consequences of exogenous intoxications are nowadays better apprehended especially regarding alcohol. Alcoholism during pregnancy is the cause of the syndrome of foetal alcoholism described in France by Lemoine in 1968 and then by Jones and Smith in 1973. The prevalence of the table is 1 out of 700 to 800 deliveries for the severe forms and concerns especially by not exclusively the most underprivileged sections of the population and shows in: -- a very specific dysmorphy of skull and face and other abnormalities which give to the face a singular and persistent aspect; -- various and frequent malformative abnormalities with a pronounced tendency for cardiopathy. Most of them are latent or of late discovery; -- a constant growth lateness which is also part of the table as well as prematurity and spontaneous abortion. Hypotrophy is moderate, total, and cerebral; -- effects on central nervous system: it is the third overall cause of mental lateness after trisomy and deficiency of neural canal. Other causes and themselves to alcohol to produce these effects that show themselves on badly affected children or dead in utero because of macroscopic and microscopic alterations of numerous cerebral structures. From a clinical view point, they show themselves by abnormalities of the neural canal, a decreasing of the crane perimeter, neonatal neurologic troubles due to deficiency in the first hours of life, followed during the second and third day by a table evoking a weaning syndrome. The evolution on a medium term is characterized by the persistence of the crane and skull dysmorphy modified by parents phenotype, a persistence of the growth lateness leading to dwarfism in the severe forms. In the moderate and medium form thinness and paleness are spectacular and malformations exist in 2/3 of the cases. The neurologic and behaving evolution is documented by some prospective studies. They tend to indicate the persistence for the severe forms of troubles concerning hyperactivity, lack of attention and decreasing of the crane perimeter as well as a main mental lateness in half of the cases. The study made in Roubaix shows that behaving and intellectual troubles are more pronounced when the dysmorphy is marked. The effects of alcohol lead to a syndrome of foetal alcoholism when the level of alcoholization is high which correspond to K. Sulik's experimental data in 1982. On the other hand, a relation dose-effect has not been yet demonstrated except for hypotrophy. This is the same for threshold-dose. There is no residual effects confirming that alcoholism and its intensity during pregnancy have a direct effect upon descendants. As a matter of fact after weaning and recovery children are again normal and normotroph. Pregnancy and especially delivery are privileged period for detection of maternal alcoholism and beginning of a prevention in a view to avoid. These effects during a later pregnancy.(ABSTRACT TRUNCATED AT 400 WORDS)

Alcoholism↗

PubMed1987

Distinct mechanisms regulate MHC class II gene expression in B cells and macrophages.

In a previous series of studies, we had shown that the constitutive Ia expression in an immunoselected Ia-human B cell variant, RJ 2.2.5, could be restored by somatic cell hybridization with mouse B cells. These experiments allowed us to show the existence of a transacting activator factor(s) operating across species barriers and encoded by the aIr-1 locus located on mouse chromosome 16. The aim of the present study was to investigate whether the B cell constitutive Ia expression and the inducible Ia expression, as seen in macrophages treated with IFN-gamma, are controlled by similar intracellular factors. To this purpose, we constructed an interspecies somatic cell hybrid between the human Ia-RJ 2.2.5 B cells and the mouse Ia-P388 D1 macrophage cells. These murine cells transiently express Ia antigens when incubated with IFN-gamma. Our results show that RJ 2.2.5 X P388 D1 cell hybrids do not express either human or mouse class II gene products. Treatment with human recombinant IFN-gamma did not modify the MHC phenotype of either the hybrid cells or the human parental cells. On the other hand, treatment of the hybrid cells with murine recombinant IFN-gamma resulted in de novo expression of mouse Ia mRNA and corresponding cell surface antigens without, however, reinduction of the human class II-positive phenotype. Furthermore, treatment with the mouse lymphokine significantly increased the levels of human HLA class I mRNA and corresponding cell surface antigens in the hybrid cells, further reinforcing the notion of the existence of non-species-specific secondary mediators generated after receptor-ligand interaction in the IFN-gamma system. Together, these results indicate that in macrophages, the intracellular events taking place after binding of IFN-gamma with its own receptor and leading to the expression of a class II-positive phenotype do not operate via an activation of the aIr-1 locus and/or its products. Thus, at least in our experimental system, we can firmly establish a first, relevant distinction between constitutive and inducible class II gene expression. This difference, dictated by the specific differentiation program of each cell type, may be relevant for the understanding of the function of class II gene products.

Animals↗

PubMed1993

Novel control of the position-dependent expression of genes in hepatocytes. The GLUT-1 transporter.

The basal hepatocyte phenotype is conferred by the expression of liver-specific genes. In the adult liver, the basal hepatocyte phenotype is further modified by transcriptional and post-transcriptional regulation of genes which result in the appearance of specific proteins in selected hepatocytes. One of these proteins is the erythroid/brain or GLUT-1 glucose transporter. The GLUT-1 protein is detected in the plasma membrane of only one or two hepatocytes located at the end of the liver cell plate, contiguous to the hepatic venule. The objective of this study was to define the molecular mechanisms responsible for the restricted expression of the GLUT-1 protein in rat liver. Hepatocytes were isolated from either the proximal ("periportal") or the distal ("perivenular") half of the liver cell plate. The GLUT-1 mRNA as well as the GLUT-1 protein content and intracellular distribution were defined after subcellular fractionation of each hepatocyte population. In addition, the location of the GLUT-1 protein in liver tissue was determined by confocal microscopy. We propose that the GLUT-1 gene is transcribed and the mRNA is translated by both "periportal" and "perivenular" hepatocytes. However, insertion of the GLUT-1 protein into the plasma membrane occurs only in the last two hepatocytes contiguous to the hepatic venule. In other hepatocytes, the protein remains in a different cellular compartment characterized here as a "low density microsomal" fraction.

Animals↗

PubMed1995

Internalization of Candida albicans and cytoskeletal organization in macrophages and fibroblasts treated with concanavalin A.

This paper investigates the ability of macrophages and of non-typically phagocitic cells such as fibroblasts to internalize 51Cr-labelled C. albicans in presence or in absence of lectin concanavalin A (Con A). The results obtained demonstrate that fibroblasts are also able to internalize C. albicans and that this property is potentiated by the presence of Con A. Lectin modifies only the phenotype of the fibroblast, which, poorly attached to the substrate, is globular in shape. Despite reduced cellular spreading, phagocytosis is stimulated by the lectin. In both cell populations, changes in the organization of some cytoskeletal proteins such as tubulin, actin and alpha-actinin are evident during the C. albicans infection; such rearrangements are more evident and longlasting in the fibroblasts treated with Con A.

Actinin↗