No abstract available.
Animals ; Neurons* ; Rats*

No abstract available.
Animals ; Rats* ; Somatotrophs*

No abstract available.
Animals ; Growth Hormone* ; Prolactin* ; Rats*

No abstract available.
Animals ; Gonadotropin-Releasing Hormone* ; Rats*

Some of the pituitary prolactinomas were reported that they don't have active dopamine receptors and do not respond to bromocriptine which is a dopamine agonist. GH3 cell line which is derived from the rat pituitary tumor cells lacks affinity of dopamine receptors and secrete prolactin as well as small amount of growth hormone. Although it has been reported that epidermal growth factor (EGF) induces functional expression of dopamine receptors on GH3 cells in vitro, there has been a contradictory result. In the present study, EGF effect on the GH3 cell response to the bromocriptine was observed in order to investigate whether EGF induces dopamine receptor expression on dopamine resistant tumors in the absence of serum. GH3 cells were cultured for 4 days in the serum-supplemented medium (SSM) followed by culture in serum-free medium (SFM) with or without EGF. Additionally, effect of tamoxifen was also observed. EGF decreased the cell number and the ratio of cell division of GH3 cells while the ratio of prolactin-immunoreac-tive cells was increased. However, EGF did not show any significant effect on the GH3 cell response to bromocriptine treatment. Although tamoxifen decreased the GH3 cell number by increasing apoptosis, it did not influence GH3 cell response to bromocriptine. Our results indicate that EGF does not increase the affinity of dopamine receptors on GH3 cells and is not useful for the treatment of the dopamine-resistant prolactinoma.
Animals ; Apoptosis ; Bromocriptine ; Cell Count ; Cell Division ; Cell Line ; Dopamine ; Dopamine Agonists ; Epidermal Growth Factor* ; Growth Hormone ; Pituitary Neoplasms ; Prolactin ; Prolactinoma ; Rats ; Receptors, Dopamine ; Tamoxifen

This study was performed to investigate the effect of progesterone (P) on the estrogen-induced proliferation of mammotropes in cultures of normal rat pituitary cells. Dispersed pituitary cells from male rats were cultured in Dulbecco's Modified Eagle's medium containing striped 10% fetal bovine serum for 6 days. Part of cells were treated with 10(-9) M 17beta-estradiol with or without P (10(-6) M). For the simultaneous detection of mitotic cells and mam-motropes, bromodeoxyuridine (BrdU) labeling and double immunocytochemical staining for BrdU and prolactin were performed. The ratio of BrdU-labeled cells among mammotropes (BLI) was increased by 6.3-fold after 6 day treatment with estradiol, which was partly suppressed by 2.3-fold by additional P treatment. The percentage of mammotropes among pituitary cells was increased by 1.5-fold by estradiol treatment, which was suppressed by 1.1-fold after coadminis-tration of progesterone. Thus, coadmistration of progesterone could suppress the estradiol-induced effect on the BLI and the proportion of mammotropes by 75% and 80%, respectively. In addition, apoptotic ratio of mammotropes was not changed by hormone treatment. The present data demonstrated that progesterone inhibits estradiol-induced proliferation of mammotropes, which may contribute to the decrease in the proportion of mammotrope. The indirect modulatory effect of progesterone on the estradiol-induced increase in the prolactin secretion in the rat pituitary was suggested.
Animals ; Bromodeoxyuridine ; Estradiol ; Estrogens* ; Humans ; Male ; Progesterone* ; Prolactin ; Rats*

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)induces apoptosis in some cancer cells such as breast,prostate,lung,and colon cancer cells,but not normal cells.However,because the effects of TRAIL in gastric cancer cells is unclear,we undertook this study to clarify the effects of TRAIL and its mechanism. To assess the cytotoxicity of TRAIL,two human gastric cancer cell lines,SNU-484 and SNU601,were treated with TRAIL (0-200 ng/mL)in the presence or absence of cycloheximide (1 microgram/mL)for 24 h.Both SNU-484 and SNU-601 were sensitive to TRAIL-induced cell death in a dose-dependent manner.The combination of TRAIL (100 ng/mL)and cycloheximide (1 microgram/mL)for 24 h enhanced cell death and PARP cleavage by promoting activations of caspase-8, caspase-9,and caspase-3,relative to that of TRAIL alone.We further examined the expressions of death receptor 4 (DR4),death receptor 5 (DR5),and FLICE inhibitory protein (FLIP).Although DR4 and DR5 were expressed in both cell lines,the expression of long form (FLIPL )and short form (FLIPS )of FLIP were detected at the low levels. Overexpression of FLIPL or FLIPS in both cell lines rendered the cells resistant to TRAIL.Taken together,our results suggest that FLIP promotes human gastric cancer cell survival against TRAIL-induced apoptosis and is important modulator for TRAIL-induced cell death in human gastric cancer cells.
Apoptosis ; CASP8 and FADD-Like Apoptosis Regulating Protein ; Caspase 8 ; Cell Death ; Cell Line ; Cell Survival ; Colonic Neoplasms ; Cycloheximide ; Humans* ; Necrosis* ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; Stomach Neoplasms*

Apoptosis is a genetically programmed cell death that is required for morphogenesis during embryogenic development and for tissue homeostasis in adult organisms. Although apoptosis is important in the development, expression of apoptosis-related genes has been studied mostly in the cancers and neurodegenerative diseases. We intended to obtain the basic data in order to understand the role of the apoptosis-related genes including bcl-2 in the apoptosis in the human development. Immunohiostochemistry for Bcl-2 was performed using Korean fetal lung, kidney, thymus, placenta, testis, small intestine, pancrease, skin, urinary bladder tissues in the 14~30 weeks of the human development. Our results showed that Bcl-2 appeared in early stages of human development in the lung, kidney, thymus, placenta, small intestine, pancreas. As differentiation grew, expression of Bcl-2 decreased and had the tendency of localizing in the bronchial epitheliums, tubular epitheliums, Bowman's epithelium, lymphocytes, synchytial trophoblasts, intestinal epitheliums, ganglionic cells, ductal epitheliums of pancreas. We suggested that in the early stages when differentiation didn't occur cell death was suppressed, in the late stages when differentiation was achieving cell death increased to remove the innecessary portions of the organs to protect the specific cells of the organs having functions. For the efficiency of the experiment, a high-throughput technique, a tissue-array method was applied which contributed to save time, money and labor without performance errors. Tissue-array technique will be useful to fasten the developmental studies.
Adult ; Male ; Female ; Humans

No abstract available.
Animals ; Brain* ; Mice*

No abstract available.
Animals ; Rats* ; Suprachiasmatic Nucleus* ; Vasoactive Intestinal Peptide*