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L Tseng

Publications and source records attributed to L Tseng.

89 records · Page 5Linked to original sources
PubMed1975

Comparison of results from in situ and in vitro perfusions of rabbit uterus with labeled estrone and estradiol.

The interconversion of labeled estrone (E1) and estradiol (E2) in rabbit uterus was studied in vivo and in vitro, in order to evaluate the influence of incubation conditions upon the preferred direction of the reversible conversion of E2 to E1. In a typical experiment, one uterine horn was perfused intraluminally in situ with a mixture of [3H]E2 and [14C]E1, while the other horn was dissected and used for in vitro perfusions with the same tracers, both intraluminally and on tissue slices. The ratios of rate constants corresponding to the oxidative and reductive reactions were found to be similar under the three perfusion conditions, as calculated from the isotopic data. The rate constant of conversion of E1 to E2 was 10-20 times larger than the rate constant of the opposite reaction. Equal E2 nuclear saturation levels were obtained by perfusion of the uterine tissue with excess [3H]E2 in situ and in vitro after slicing.

Animals↗
PubMed1975

Effects of progestins on estradiol receptor levels in human endometrium.

Medroxyprogesterone acetate (Provera) was administered orally during 2-4 days to women undergoing endometrial curettage during the follicular phase of the menstrual cycle. Estradiol (E2) receptor levels were estimated from the amounts of 2H-E2 tightly bound in nuclei after incubation of endometrial tissue with an excess of the labeled hormone. An average value (9 subjects) of 1.5 pmole E2/mg DNA +/- 0.7 (mean +1- SD) was found. This value is significantly lower than the average E2 receptor levels in proliferative endometrium of untreated subjects (3.2 +/- 1.3, n = 33) and equals the level observed in the early secretory phase (1.5 +/- 0.5, n = 5). These results indicate that one of the progestin effects on human endometrium is the reduction of E2 receptor levels.

Adult↗
PubMedDate not supplied

Cyclic expression of endothelial nitric oxide synthase mRNA in the epithelial glands of human endometrium.

OBJECTIVES: Nitric oxide synthase (NOS), responsible for the synthesis of nitric oxide (NO), is the key enzyme that regulates the NO-mediated biologic functions in various types of tissue. We believed that NO may be involved in regulating the development of the microvascular system and vascular tone in human endometrium. However, the biology of NOS in this system remains poorly understood. To determine the paracrine action of NOS derived from endometrial cells on vascular blood flow, the first task is to identify NOS in endometrial cells. This study was undertaken to examine whether human endometrial cells would express endothelial or inducible NOS (eNOS or iNOS). In addition, we examined the cell-specific expression of eNOS. METHODS: Beta nicotinamide adenine dinucleotide reduced from (NADPH)-diaphorase histochemistry assay was carried out in human endometrial specimens (n = 4). Nitric oxide synthase mRNA expression was studied in intact tissue (n = 4), isolated epithelial glands (n = 25), and stromal cells (n = 10). Northern blot and solution hybridization/ribonuclease protection assay with specific RNA probes transcribed from human eNOS and iNOS cDNA were used to identify NOS mRNAs. RESULTS: NADPH-diaphorase histochemistry selectively labeled epithelial glands in the late secretory phase. Northern blot analysis revealed that glandular cells expressed a single size of eNOS mRNA (4.5 kb) but no detectable iNOS. Endothelial NOS mRNA was expressed in epithelial glands, but it was not detectable in stromal cells. The relative amount of eNOS in epithelial glands isolated from specimens (n = 23) at various stages of menstrual cycle were analyzed using a solution hybridization assay. The levels of eNOS mRNA varied among specimens. Epithelial glands from early secretory endometrium showed greater expression of eNOS mRNA. The highest eNOS expression was found in the glands of late secretory endometrium. In contrast, iNOS was detected only in the epithelial glands of a menstrual endometrium. CONCLUSION: This study demonstrated that NADPH-diaphorase activity is highly concentrated in the epithelial glands of late secretory endometrium. Expression of eNOS mRNA is enhanced in the glands of early secretory endometrium. The strongest expression resides in the epithelial glands of late secretory endometrium. This observation suggests that regulation of eNOS may be a physiologic response to steroid hormones and locally produced peptide hormones in the endometrial environment. It also suggests that NO may play a role in the onset of menses.

Cells, Cultured↗
PubMedDate not supplied

Progestin, estrogen, and insulin-like growth factor-I stimulate the prolactin receptor mRNA in human endometrial stromal cells.

OBJECTIVE: To identify the expression of the prolactin receptor (PRL-R) mRNA in human endometrial stromal and glandular epithelial cells in order to ascertain the autocrine/paracrine actions of PRL and to determine the effect of steroid hormones and growth factor on PRL-R mRNA during decidualization. METHODS: Human endometrial stromal cells and glandular epithelial cells were isolated from tissue fragments by collagenase digestion and total RNA was isolated. Stromal cells were cultured with or without progesterone (P) or medroxyprogesterone acetate (MPA) for various periods of time. Prolactin receptor and its mRNA were determined by Western blot analysis and solution hybridization/ribonuclease protection assay. The effects of estrogen, insulin-like growth factor (IGF)-I, and PRL on PRL-R mRNA were also studied. RESULTS: Both types of endometrial cells expressed PRL-R mRNA. Prolactin receptor mRNA content in glandular cells was consistently much less than that in stromal cells (1 versus 5-12). Progesterone or MPA stimulated the PRL-R mRNA expression two- to greater than ten-fold in the stromal cells of eight endometrial specimens. Stimulation by progestin was concentration dependent and required at least 1-2 days' incubation. A high level of PRL-R mRNA was maintained in stromal cells beyond 10 days' incubation with progestin. The stimulatory effect of progestin was inhibited by RU 486 and by cycloheximide, suggesting that progestin-receptor interaction and de novo protein synthesis mediate the up-regulation. In addition, estradiol and IGF-I stimulated PRL-R mRNA. Western blot analysis showed that progestin increased the PRL-R protein. A 90-kd band previously identified as PRL-R was ubiquitously distributed in the soluble and particulate fractions of the stromal cells. CONCLUSION: This study demonstrated that PRL-R mRNA is expressed in both types of endometrial cells and that PRL-R mRNA and its protein are up-regulated by progestin, estrogen, and IGF-I during decidualization of endometrial stromal cells.

Cells, Cultured↗
PubMedDate not supplied

Dopamine and morphine stimulate nitric oxide release in human endometrial glandular epithelial cells.

OBJECTIVE: Previous studies have shown that human endometrial glandular epithelial cells contain endothelial nitric oxide synthase indicating that the endometrium might produce nitric oxide (NO). We conducted this study to identify stimuli that can activate a transient NO release from endometrial glandular epithelial cells because NO is an important intracellular and intercellular signal transduction pathway in reproductive cycle. METHODS: Endometrial glandular epithelial cells, free of endothelial cells, were isolated from human endometrial specimens and maintained viable in RPMI 1640 medium with 2% fetal bovine serum for 2-4 days. Nitric oxide release from the glandular cells in response to stimuli was monitored continuously amperometrically. RESULTS: Among the substances examined, we found that dopamine and morphine stimulated a transient surge of NO production that was dose-dependent, whereas estrogen, progesterone, or relaxin (RLX) had no short-term effect on NO release. Cells treated with RLX or dopamine for 4 days enhanced the dopamine-induced NO release fourfold to sixfold, with the peak of the NO surge shifting from 35 to 15 seconds. CONCLUSION: Endometrial glandular cells were capable of producing NO. Dopamine and morphine were potent stimuli for a transient surge of NO release from endometrial glandular cells. Furthermore, prolonged exposure to dopamine or RLX enhanced the sensitivity of NO release in endometrial glands.

Animals↗