Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.4 (trypsin)
 42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We measured phosphatidylcholine secretion and its response to surfactant secretagogues in type II cells from developing rats. Cells were isolated from fetal rats on day 21 of gestation by digestion with collagenase and trypsin and purification by differential adhesion. Cells were isolated from adult and postnatal rats on days 1, 7, 14, and 30 by elastase digestion and panning on immunoglobulin G-coated dishes. The basal rate of phosphatidylcholine secretion was the same at all ages but there were developmental changes in the response to secretagogues. The response to terbutaline and an adenosine A2 receptor agonist increased from fetal life until day 7 when it reached the level of adult cells. Adenosine deaminase did not increase the response of the cells to these agonists until day 30, suggesting that the adenosine A1 receptor inhibiting secretion does not become functional until that age. The response to 12-O-tetradecanoylphorbol 13-acetate was lower in the fetal cells but had reached the adult level by day 1. The developmental increase in the response of the cells to ATP was more prolonged with the maximum response not being attained until day 30. With the exception of day 30, when the response to most of the secretagogues was very high, the response to ionomycin was the same at the other ages. These data suggest differential maturation of the signal-transduction pathways mediating surfactant secretion in type II cells.
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PMID:Ontogeny of surfactant secretion in type II pneumocytes from fetal, newborn, and adult rats. 155 Feb 57

Platelets and platelet-conditioned medium (PCM) decrease endothelial protein permeability in vitro. Adenosine and a > 100-kDa protein have previously been implicated as the soluble factors released from platelets that decrease endothelial permeability. The objective of this study was to further investigate the role of adenosine in this platelet response. Measurements of adenosine and its precursor adenine nucleotides by high-performance liquid chromatography were correlated with the assessment of permeability by 125I-labeled albumin clearance and electrical resistance across endothelial cell monolayers derived from the bovine pulmonary artery. PCM contained micromolar concentrations of AMP, ADP, and ATP, but adenosine was below detectable levels (< or = 0.1 microM). Adenosine deaminase, an enzyme that converts adenosine to inactive inosine, or an adenosine-receptor antagonist did not block the platelet- or PCM-mediated decrease in endothelial permeability. A < 3-kDa fraction of PCM that contained micromolar concentrations of AMP and ADP did not affect endothelial permeability, whereas a > 3-kDa fraction that contained much reduced levels of AMP and ADP significantly decreased permeability. This activity of PCM was sensitive to insoluble trypsin. This study rules out adenosine and adenine nucleotides as primary factors in the platelet-induced decrease in endothelial permeability and suggests that the active factor is a protein.
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PMID:Protein, not adenosine or adenine nucleotides, mediates platelet decrease in endothelial permeability. 937 67