scholarly journals Taurine Down-Regulates Basal and Osmolarity-Induced Gene Expression of Its Transporter, but Not the Gene Expression of Its Biosynthetic Enzymes, in Astrocyte Primary Cultures

2002 ◽  
Vol 75 (3) ◽  
pp. 919-924 ◽  
Author(s):  
Marc Bitoun ◽  
Marcel Tappaz
Keyword(s):  
Gene Expression ◽  
Primary Cultures ◽  
Biosynthetic Enzymes

Gene expression of catecholamine biosynthetic enzymes following exercise: modulation by age

Neuroscience ◽  
2001 ◽  
Vol 103 (3) ◽  
pp. 703-711 ◽  
Author(s):  
N. Tümer ◽  
H.A. Demirel ◽  
L. Serova ◽  
E.L. Sabban ◽  
C.S. Broxson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Biosynthetic Enzymes

scholarly journals Comparative activity of pulsed or continuous estradiol exposure on gene expression and proliferation of normal and tumoral human breast cells

2002 ◽  
Vol 28 (3) ◽  
pp. 165-175 ◽  
Author(s):  
V Cavailles ◽  
A Gompel ◽  
MC Portois ◽  
S Thenot ◽  
N Mabon ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Lines ◽  
Hormone Replacement ◽  
Primary Cultures ◽  
Continuous Treatment ◽  
Luciferase Reporter ◽  
Breast Cancer Cell Lines ◽  
Human Breast ◽  
Kinetic Profile ◽  
Breast Cells

Intranasal administration of hormone replacement therapy presents an original plasma kinetic profile with transient estrogen levels giving rise to the concept of pulsed therapy. To further understand the molecular effects of this new therapy, we have compared the effects of pulsed and continuous estradiol treatments on two critical aspects of estradiol action: gene expression and cell proliferation. Cells were stimulated with estradiol as 1-h pulsed or 24-h continuous treatments at concentrations such that the 24-h exposure (concentration x time) was identical in both conditions. In MCF7 cells, the transcriptional activity of estrogen receptors (ER) on a transiently transfected responsive estrogen response element-luciferase reporter construct was shown to be drastically (approximately 10-fold) and similarly stimulated after both treatments. Moreover, the increased mRNA expression of three representative estradiol-sensitive genes (pS2, cathepsin D, progesterone receptor), evaluated by Northern blot, was identical after 1-h pulse with 7 nM estradiol or continuous treatment with 0.29 nM estradiol with the same kinetic profile over 48 h. Proliferation was quantified by a histomorphometric method on primary cultures of human normal breast cells from reduction mammoplasties and using a fluorescence DNA assay in six human breast cancer cell lines which were ER positive or negative. After a 7-day treatment period, estradiol had no effect on the proliferation of the three ER negative cell lines (BT20, MDA MB231, SK BR3) but significantly stimulated the proliferation of the normal cells and of the three tumoral hormone-sensitive cell lines (MCF7, T47D, ZR 75-1); both hormone treatments producing the same increases in cell growth. In conclusion, we have shown that the genomic or proliferative effects of estradiol were identical with pulsed or continuous treatments, thus indicating that estrogenic effects are not strictly related to concentrations but rather to total hormone exposure.

CFTR ΔF508 mutation has minimal effect on the gene expression profile of differentiated human airway epithelia

2005 ◽  
Vol 289 (4) ◽  
pp. L545-L553 ◽  
Author(s):  
Joseph Zabner ◽  
Todd E. Scheetz ◽  
Hakeem G. Almabrazi ◽  
Thomas L. Casavant ◽  
Jian Huang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cystic Fibrosis ◽  
Large Scale ◽  
Expression Profiles ◽  
Expression Patterns ◽  
Primary Cultures ◽  
Gene Expression Profiles ◽  
Filter Method ◽  
Tissue Destruction ◽  
Airway Epithelia

Cystic fibrosis (CF) is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR), an epithelial chloride channel regulated by phosphorylation. Most of the disease-associated morbidity is the consequence of chronic lung infection with progressive tissue destruction. As an approach to investigate the cellular effects of CFTR mutations, we used large-scale microarray hybridization to contrast the gene expression profiles of well-differentiated primary cultures of human CF and non-CF airway epithelia grown under resting culture conditions. We surveyed the expression profiles for 10 non-CF and 10 ΔF508 homozygote samples. Of the 22,283 genes represented on the Affymetrix U133A GeneChip, we found evidence of significant changes in expression in 24 genes by two-sample t-test ( P < 0.00001). A second, three-filter method of comparative analysis found no significant differences between the groups. The levels of CFTR mRNA were comparable in both groups. There were no significant differences in the gene expression patterns between male and female CF specimens. There were 18 genes with significant increases and 6 genes with decreases in CF relative to non-CF samples. Although the function of many of the differentially expressed genes is unknown, one transcript that was elevated in CF, the KCl cotransporter (KCC4), is a candidate for further study. Overall, the results indicate that CFTR dysfunction has little direct impact on airway epithelial gene expression in samples grown under these conditions.

scholarly journals Peroxisome Proliferator-Activated Receptor-α Control of Lipid and Glucose Metabolism in Human White Adipocytes

Endocrinology ◽  
2010 ◽  
Vol 151 (1) ◽  
pp. 123-133 ◽  
Author(s):  
Carole Ribet ◽  
Emilie Montastier ◽  
Carine Valle ◽  
Véronic Bezaire ◽  
Anne Mazzucotelli ◽  
...  
Keyword(s):  
Gene Expression ◽  
Biological Effects ◽  
Primary Cultures ◽  
Lactate Production ◽  
De Novo Lipogenesis ◽  
Peroxisome Proliferator ◽  
Palmitate Oxidation ◽  
White Adipocytes ◽  
Pparγ Agonist ◽  
Pparα Agonist

Abstract This work aimed at characterizing the role of peroxisome proliferator-activated receptors (PPAR)α in human white adipocyte metabolism and at comparing PPARα and PPARγ actions in these cells. Primary cultures of human fat cells were treated with the PPARα agonist GW7647 or the PPARγ agonist rosiglitazone. Changes in gene expression were determined using DNA microrrays and quantitative RT-PCR. Western blot and metabolic studies were performed to identify the biological effects elicited by PPAR agonist treatments. GW7647 induced an up-regulation of β-oxidation gene expression and increased palmitate oxidation. Unexpectedly, glycolysis was strongly reduced at transcriptional and functional levels by GW7647 leading to a decrease in pyruvate and lactate production. Glucose oxidation was decreased. Triglyceride esterification and de novo lipogenesis were inhibited by the PPARα agonist. GW7647-induced alterations were abolished by a treatment with a PPARα antagonist. Small interfering RNA-mediated extinction of PPARα gene expression in hMADS adipocytes attenuated GW7647 induction of palmitate oxidation. Rosiglitazone had no major impact on glycolysis and β-oxidation. Altogether these results show that PPARα can selectively up-regulate β-oxidation and decrease glucose utilization in human white adipocytes.

Insulin-like growth factor I gene expression by primary cultures of ovarian cells: insulin and dexamethasone dependence.

Endocrinology ◽  
1993 ◽  
Vol 132 (6) ◽  
pp. 2703-2708 ◽  
Author(s):  
L F Botero ◽  
C T Roberts ◽  
D LeRoith ◽  
E Y Adashi ◽  
E R Hernandez
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Primary Cultures ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Ovarian Cells ◽  
Growth Factor I ◽  
I Gene

Transferrin gene expression and transferrin immunolocalization in developing foetal rat lung

1991 ◽  
Vol 99 (3) ◽  
pp. 651-656 ◽  
Author(s):  
S.J. Skinner ◽  
C.E. Somervell ◽  
S. Buch ◽  
M. Post
Keyword(s):  
Gene Expression ◽  
Extracellular Matrix ◽  
Epithelial Cells ◽  
Chondroitin Sulphate ◽  
Primary Cultures ◽  
Basement Membranes ◽  
Lung Cells ◽  
Intense Staining ◽  
Tf Gene ◽  
Foetal Lung

In previous studies we have shown that transferrin (Tf) specifically stimulates dermatan- and chondroitin-sulphate proteoglycan accumulation around lung cells, and in the extracellular matrix of lung tissue, in vitro. The aim of this study was to determine whether the gene for Tf was activated in specific lung cells during development, and whether the protein product showed evidence of association with extracellular matrix. The expression of the gene in developing lung was shown by the hybridization of a Tf cDNA to a 2.4 kb (kilobase) mRNA species in total RNA extracts of foetal lung. The expression of the Tf gene in comparison to a control gene (GAPD, glyceraldehyde phosphate dehydrogenase) was greatest in 19, 20 and 21 day foetal lung, rising from low levels on day 18 and decreasing markedly at term (day 22). Extracts of RNA from primary cultures of mesenchymal fibroblasts and type II epithelial cells were also analysed for Tf mRNA. These experiments indicated that Tf gene expression was predominantly confined to the mesenchymal compartment. The presence of Tf in histological sections of foetal lung was demonstrated by immunohistochemistry and showed a distinct pattern, with intense staining of the alveolar and the capillary basement membranes. The matrix surrounding the mesenchymal fibroblasts was stained in a diffuse network while epithelial cells were unstained. The staining was low from days 12–16 of gestation, increased to a maximum at days 19–20 but decreased markedly toward term. The Tf staining did not co-localize with transferrin receptor, also demonstrated by immunohistochemistry. These results suggest that Tf is not only present at specific sites in the developing lung, but also is synthesized according to a strict developmental schedule of gene expression.

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