Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.36 (hyaluronidase)
 4,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

High density lipoprotein (HDL3) binds with high affinity to many types of cells, but controversy exists concerning the nature and biological significance of the binding. We have recently demonstrated that HDL and apoproteins (apo)-AI, -AII, and -CI stimulate a specific and dose-dependent increase in placental lactogen (hPL) release from human trophoblast cells. To examine the possible relationship between HDL3 binding and stimulation of hPL release, we have characterized the binding of [125I]HDL3 to an enriched fraction of hPL-producing trophoblast cells. Binding studies were performed on trophoblast cells isolated by isopycnic centrifugation of collagenase/hyaluronidase-dispersed placental tissue and apo-E free-HDL3 (density, 1.125-1.215 g/ml). Scatchard analysis of binding studies performed at 37 C for 2 h revealed two classes of binding sites: 1) high affinity binding sites with a Kd of 9.7 +/- 2.2 micrograms/ml (1.3 x 10(-7) M) and 9.8 +/- 3.2 x 10(5) binding sites/trophoblast cell, and 2) low affinity binding sites with a Kd of 172.8 +/- 64.8 micrograms/ml (2.3 x 10(-6) M) and an estimated 3.2 x 10(6) sites/cell. As has been found in hepatocytes and other cells, the number of HDL3-binding sites per trophoblast cell (but not the binding affinity) decreased at lower incubation temperatures. In addition, HDL3 binding to trophoblasts cells did not require calcium and was not affected by prior treatment of the cells with pronase or trypsin. HDL3-binding sites on trophoblast cells, however, were not specific for HDL3. Low density lipoprotein (density, 1.063-1.055 g/ml), which does not stimulate hPL release, was nearly as potent on a molar basis as HDL3 in binding to the high and low affinity binding sites on trophoblast cells. Furthermore, nitrated HDL3, which does not compete for high affinity binding to trophoblast cells, stimulated hPL release. Although the characteristics of HDL3 binding to trophoblast cells are similar to those of other cells, these results strongly suggest that the binding of HDL3 to high affinity binding sites is not essential for HDL-mediated hPL release.
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PMID:High density lipoprotein3 binding and biological action: high affinity binding is not necessary for stimulation of placental lactogen release from trophoblast cells. 258 47

The dynamics of the release of human placental lactogen (hPL) under basal conditions and response to various secretogogues has been studied in perifused enriched hPL-producing cells from term placentae prepared by the isopycnic centrifugation of collagenase/hyaluronidase-dispersed placental cells on Percoll gradients. Under basal conditions, the perifused cells released hPL at a relatively constant rate for up to 24 h in culture. The mean rates of hPL release from cells (5 x 10(6) cells) from 18 normal full-term placentae varied from 1.8 to 20.2 ng/5 min (mean 7.7 ng/5 min). The cells from term placentae, however, did not release detectable amounts of chorionic gonadotrophin or the cytosolic enzymes lactic dehydrogenase and alkaline phosphatase. The amounts of hPL released by the perifused cells were inversely related to cell density with mean rates of hPL release by 2, 5, and 10 x 10(6) cells of 15.8, 8.6, and 5.7 ng/10(6) cells/0.5 h. The perifused cells responded to provocative stimuli (high-density lipoproteins (HDL), apolipoproteins AI, AII, and CI, partially purified hPL-releasing factor, phorbol esters, sn-1,2-diacylglycerol, and cAMP) in a manner qualitatively similar to enriched trophoblast cells and placental explants in static culture. Release of hPL in response to HDL, apoproteins AI, AII, and CI, and partially purified hPL-releasing factor was dose-dependent and occurred within 5 min of exposure. Basal and stimulated hPL release by perifused trophoblast cells that had been previously frozen at -70 degrees C for four weeks was identical to that of freshly dispersed cells from the same placenta. These experiments indicate that perifused trophoblast cells may be used as a model system to examine the dynamics of hPL release under basal conditions and in response to provocative stimuli.
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PMID:Characterization of placental lactogen release from perifused human trophoblast cells. 339 89

An enriched fraction of human placental cells that synthesize and release both placental lactogen (hPL) and hCG was obtained by isopycnic centrifugation of collagenase/hyaluronidase-dispersed cells through a density gradient of 40% Percoll. The enriched cells, which banded at a density of approximately 1.01 g/ml, comprised 10-15% of the total DNA. During the first 24 h after attachment, the cells released 50-250 ng hPL and 4-10 mIU hCG/10(6) cells. Thereafter, the rate of hPL release decreased, while the rate of hCG and [35S]trichloroacetic acid-precipitable protein release remained constant. The enriched cells responded to phospholipase A2, low extracellular calcium, and (Bu)2cAMP in a manner similar to that of placental explants. Phospholipase A2 (0.1 and 1 U/ml) stimulated hPL release by 270% and 568%, respectively, and low extracellular calcium (0-0.18 mM) stimulated hPL release by 48%. (Bu)2 cAMP (1 mM) stimulated hCG release by 42%, but had no effect on hPL. Estradiol (10(-5)-10(-12) M) and progesterone (10(-5)-10(-10) M) had no effect on the synthesis and release of either hPL or hCG over a 6-day period. In addition, insulin (8.3 X 10(-7) M) and changes in medium glucose content (0-5 mg/ml) had no effect on hPL release over a 72-h period. Since the enriched trophoblast cells respond to provocative stimuli in a manner similar to that of explants and placental fragments, this cell population is a useful model system for investigations of the cellular mechanisms of hPL and hCG release.
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PMID:Characterization of the synthesis and release of human placental lactogen and human chorionic gonadotropin by an enriched population of dispersed placental cells. 630 87