scholarly journals Potentiation by cholera toxin of bradykinin-induced inositol phosphate production in the osteoblast-like cell line MC3T3-E1

1993 ◽  
Vol 292 (2) ◽  
pp. 401-408 ◽  
Author(s):  
Y Banno ◽  
T Sakai ◽  
T Kumada ◽  
Y Nozawa
Keyword(s):  
Cyclic Amp ◽  
Cholera Toxin ◽  
Cell Line ◽  
Inositol Phosphates ◽  
Inositol Phosphate ◽  
Receptor Protein ◽  
Osteoblastic Cell ◽  
Osteoblastic Cell Line ◽  
Inositol Phosphate Production ◽  
Receptor Number

Cells of the osteoblastic cell line MC3T3-E1 were shown to contain at least three phosphatidylinositol-specific phospholipase C (PI-PLC) isoenzymes (PLC-beta, PLC-gamma and PLC-delta) by Western blotting analysis with various anti-PLC antibodies. Stimulation of inositol phosphate production in MC3T3-E1 cells by bradykinin (BK) occurred via a GTP-binding protein. Inositol phosphate formation on stimulation by BK was not affected by pretreatment with pertussis toxin, whereas it was potentiated by cholera toxin pretreatment. Elevation of cellular cyclic AMP levels by brief pretreatment with dibutyryl cyclic AMP or forskolin failed to enhance the BK-mediated generation of inositol phosphates, but long-term preincubation with these agents partially mimicked the action of the cholera toxin. Cholera toxin also caused an increase in BK receptor number. Cycloheximide, a protein biosynthesis inhibitor, prevented the potentiating actions of the cholera toxin and the cyclic AMP-elevating agents on BK-induced inositol phosphate production, and also inhibited the increase in BK receptor number. The specific binding of [3H]BK to the whole MC3T3-E1 cells in the presence or absence of cholera toxin was completely inhibited by the B2 BK receptor antagonist D-Arg[Hyp3,Thi5,8,D-Phe7]BK, but not by the B1 BK receptor agonist des-Arg9-BK. These data suggest that the activation of PI-PLC induced by cholera toxin in BK-stimulated MC3T3-E1 cells was caused by an enhancement of the synthesis of BK receptor protein(s), at least part of which was mediated by a sustained increase in the intracellular level of cyclic AMP.

scholarly journals Cholera-toxin and corticotropin modulation of inositol phosphate accumulation induced by vasopressin and angiotensin II in rat glomerulosa cells

1988 ◽  
Vol 253 (3) ◽  
pp. 765-775 ◽  
Author(s):  
G Guillon ◽  
N Gallo-Payet ◽  
M N Balestre ◽  
C Lombard
Keyword(s):  
Angiotensin Ii ◽  
Cyclic Amp ◽  
Phospholipase C ◽  
Cholera Toxin ◽  
Inositol Phosphates ◽  
Inositol Phosphate ◽  
Dependent Manner ◽  
Intact Cells ◽  
Adp Ribosylation ◽  
Glomerulosa Cells

Vasopressin (VP) and angiotensin II (AT II) stimulate the production of inositol phosphates (IP) in rat glomerulosa cells. Guanosine 5′-[gamma-thio]triphosphate (GTP[S]), but not VP or AT II, stimulates IP production in a myo-[3H]inositol-prelabelled glomerulosa-cell membrane preparation. In combination with GTP[S], these hormones potentiate the response to GTP[S], indicating the existence of a G-protein involved in the coupling of the VP and AT II receptor with the phospholipase C. ADP-ribosylation with pertussis toxin (IAP) revealed the specific labelling of a single molecule of 41 kDa. No significant inhibition of VP- or AT II-stimulated IP accumulation was detected in intact cells when the whole 41 kDa molecule was endogenously ADP-ribosylated by IAP treatment. On the contrary, when glomerulosa cells were infected with cholera toxin (CT), both the VP- and AT II-stimulated IP accumulations were inhibited in a dose-dependent manner. Yet these effects were partial even at high concentrations of CT, and could not be related to the ADP-ribosylation of ‘alpha s’ molecules. Similarly, when the cells were infected with 1 microgram of CT/ml, the specific binding of VP and AT II decreased by 50-60%. Such results may signify that the treatment primarily affects the densities of the hormone receptors. When glomerulosa cells were incubated for 15 h in the presence of 10 nM-corticotropin (ACTH), a condition in which the intracellular concentration of cyclic AMP was increased 3-fold, the maximum IP response to 0.1 microM-VP or -AT II was decreased by 50%. When similar experiments were carried out only after a 15 min incubation period with the same concentration of ACTH, the increase in cyclic AMP was more pronounced, but no inhibition of hormone-induced IP accumulation was observed. Altogether, these results may suggest that CT exerts its action on the VP- or AT II-sensitive phospholipase C systems via a prolonged increase in intracellular cyclic AMP.

scholarly journals Thyroid-stimulating hormone stimulates increases in inositol phosphates as well as cyclic AMP in the FRTL-5 rat thyroid cell line

1987 ◽  
Vol 247 (3) ◽  
pp. 519-524 ◽  
Author(s):  
J B Field ◽  
P A Ealey ◽  
N J Marshall ◽  
S Cockcroft
Keyword(s):  
Cyclic Amp ◽  
Cell Line ◽  
Inositol Phosphates ◽  
Inositol Phosphate ◽  
Thyroid Stimulating Hormone ◽  
Thyroid Cell ◽  
Dependent Manner ◽  
Thyroid Cell Line ◽  
Rat Thyroid ◽  
Stimulating Hormone

Studies were conducted to determine whether thyroid-stimulating hormone (TSH; thyrotropin), a hormone known to increase cytosol concentrations of cyclic AMP, also stimulates the formation of inositol phosphates in thyroid cells. TSH and noradrenaline both stimulated [3H]inositol phosphate formation in a concentration-dependent manner in the rat thyroid cell line, FRTL-5 cells, which had been prelabelled with [3H]inositol. The threshold concentration of TSH required to stimulate inositol phosphate formation was more than 20 munits/ml, which is approx. 10(3)-fold greater than that required for cyclic AMP accumulation and growth in these cells. We also demonstrate that membranes prepared from FRTL-5 cells possess a guanine nucleotide-activatable polyphosphoinositide phosphodiesterase, which suggests that activation of inositide metabolism in these cells may be coupled to receptors by the G-protein, Gp. Our findings suggest that two second-messenger systems exist to mediate the action of TSH in the thyroid.

scholarly journals Influence of bacterial toxins and forskolin upon vasopressin-induced inositol phosphate accumulation in WRK 1 cells

1989 ◽  
Vol 260 (3) ◽  
pp. 665-672 ◽  
Author(s):  
G Guillon ◽  
M N Balestre ◽  
C Lombard ◽  
F Rassendren ◽  
C J Kirk
Keyword(s):  
Cyclic Amp ◽  
Cholera Toxin ◽  
Pertussis Toxin ◽  
Inositol Phosphates ◽  
Inositol Phosphate ◽  
Binding Capacity ◽  
Specific Binding ◽  
Phosphate Accumulation ◽  
Cyclic Amp Accumulation ◽  
Inositol Phosphate Accumulation

The accumulation of inositol phosphates in WRK 1 cells, stimulated with a range of vasopressin concentrations, was diminished by prior exposure to cholera toxin or forskolin, whilst that observed in the presence of maximal concentrations of the hormone was enhanced in pertussis-toxin-treated cells. In the presence of [32P]NAD+, both cholera toxin and pertussis toxin provoked the labelling of peptides with approximate Mrs of 45,000 and 41,000 respectively in the membranes of WRK 1 cells. Exposure to cholera toxin or forskolin for 15-18 h enhanced cyclic AMP accumulation in these cells. The concentrations of these agents which provoked half-maximal cyclic AMP accumulation were similar to those required to diminish receptor-mediated inositol phosphate accumulation by 50%. In contrast, half-maximal ADP-ribosylation of the 45,000Mr peptide needed 100-fold greater concentrations of the toxin than were effective in provoking half-maximal inhibition of inositol phosphate accumulation. Cholera toxin or forskolin also reduced the maximal specific binding, to intact WRK 1 cells, of both [3H][Arg8]vasopressin and the V1a antagonist [3H][beta-mercapto-beta,beta-cyclopentamethylenepropionic acid,O-methyl-Tyr2, Arg8]vasopressin. The kinetics for the loss of this binding capacity following cholera-toxin treatment were very similar to those describing the diminution of vasopressin-stimulated inositol phosphate accumulation in the same cells.

Bradykinin induces formation of inositol phosphates and causes an increase in cytoplasmic Ca2+ in the osteoblastic cell line MC3T3-E1

2009 ◽  
Vol 6 (5) ◽  
pp. 443-452 ◽  
Author(s):  
Östen Ljunggren ◽  
Hans Johansson ◽  
Sverker Ljunghall ◽  
Bertil B. Fredholm ◽  
Ulf H. Lerner
Keyword(s):  
Cell Line ◽  
Inositol Phosphates ◽  
Osteoblastic Cell ◽  
Osteoblastic Cell Line

scholarly journals Prostaglandin E receptor subtypes in mouse osteoblastic cell line.

Endocrinology ◽  
1996 ◽  
Vol 137 (5) ◽  
pp. 1698-1705 ◽  
Author(s):  
M Suda ◽  
K Tanaka ◽  
K Natsui ◽  
T Usui ◽  
I Tanaka ◽  
...  
Keyword(s):  
Cell Line ◽  
Osteoblastic Cell ◽  
Prostaglandin E ◽  
Receptor Subtypes ◽  
Osteoblastic Cell Line

scholarly journals EMMPRIN Inhibits bFGF-Induced IL-6 Secretion in an Osteoblastic Cell Line, MC3T3-E1

2017 ◽  
Vol 14 (12) ◽  
pp. 1173-1180 ◽  
Author(s):  
Akari Saiki ◽  
Mitsuru Motoyoshi ◽  
Keiko Motozawa ◽  
Teinosuke Okamura ◽  
Kousuke Ueki ◽  
...  
Keyword(s):  
Cell Line ◽  
Osteoblastic Cell ◽  
Osteoblastic Cell Line

An Electrochemical Assay for Monitoring Differentiation of the Osteoblastic Cell Line (MBA-15) on the Sensor Chip

2015 ◽  
Vol 27 (6) ◽  
pp. 1350-1358 ◽  
Author(s):  
Cigdem Yildirim-Semerci ◽  
Dafna Benayahu ◽  
Miriam Adamovski ◽  
Ulla Wollenberger
Keyword(s):  
Cell Line ◽  
Sensor Chip ◽  
Osteoblastic Cell ◽  
Electrochemical Assay ◽  
Osteoblastic Cell Line
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