Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.4.21.6 (
thromboplastin
)
13,278
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Human monocytes synthesize the protein component of
thromboplastin
and express increased procoagulant activity when appropriately stimulated in vitro. The activity reached maximum between 2 and 20 h depending on the stimulant used. The presence of lymphocytes (lymphocyte: monocyte ratio 4:1) enhanced this activity only very slightly (up to 1.3-fold) at the time of maximal monocyte
thromboplastin
expression. Lymphocytes had a marked potentiating effect on PHA stimulation that became clearly evident after 12 h, at which time the
thromboplastin
response of monocytes alone to PHA had subsided. The
thromboplastin
activity of monocytes remained at a high level for 24-40 h in the presence of PHA or endotoxin and lymphocytes, but lymphocytes did not influence the early (4-8 h)
thromboplastin
response. Neither did lymphocytes alter the magnitude or the time course of the response when monocytes were stimulated with PPD, TPA or immune complexes. The lymphoblastoid cell line Molt 4 (T cell like) was as effective as lymphocytes,
Daudi
cells (B cell like) were slightly less effective. The enhancement of
thromboplastin
activity in PHA-stimulated monocytes could be induced also by conditioned medium from PHA stimulated lymphocytes. We conclude that freshly isolated monocytes synthesize
thromboplastin
directly upon interaction with a stimulant, and are not dependent on a helper effect of lymphocytes or lymphocyte products. Such help, however, will prolong the ability of the monocytes to respond.
...
PMID:Is lymphocyte co-operation necessary for thromboplastin synthesis by human monocytes? 661 64
Endothelial cells from human umbilical veins produce a procoagulant identified as
thromboplastin
(tissue factor, factor III) when stimulated with the phorbol ester 12-0-tetradecanoyl-phorbol-13-acetate (TPA), phytohaemagglutinin (PHA) or endotoxin, Inducible
thromboplastin
synthesis (i.e. synthesis of the protein component of
thromboplastin
, apoprotein III) was totally inhibited by cycloheximide and actinomycin D, indicating that de novo protein and RNA syntheses are necessary. Serum enhanced the induced apoprotein synthesis. Of the total
thromboplastin
activity in homogenates of stimulated endothelial cells, about 50--70% was available on the cell surface for interaction with other coagulation factors, inactivation by trypsin and neutralization with antiserum against apoprotein III. Induced synthesis of
thromboplastin
in endothelial cells was 2--7-fold enhanced by the presence of several other cell types in optimal ratio 4--10 cells per endothelial cell. Some of these cell types were themselves thromboplstin producers (U-937, U-937-4), some were not inducible (lymphocytes, granulocytes and the lymphoblast lines
Daudi
and Molt 4). This enhancing effect was also seen with cell-free culture supernatants, but these were generally somewhat less effective than the intact cells. Supernatants derived from cells cultured in the presence of TPA, PHA or endotoxin were in most cases more effective than supernatants from unstimulated cells.
...
PMID:Cellular cooperation in endothelial cell thromboplastin synthesis. 684 29