scholarly journals Persistent intracellular calcium pool depletion by thapsigargin and its influence on cell growth.

1991 ◽  
Vol 266 (36) ◽  
pp. 24690-24697 ◽  
Author(s):  
T.K. Ghosh ◽  
J.H. Bian ◽  
A.D. Short ◽  
S.L. Rybak ◽  
D.L. Gill
Keyword(s):  
Cell Growth ◽  
Intracellular Calcium ◽  
Calcium Pool

scholarly journals Ca2+Pools and Cell Growth

2001 ◽  
Vol 276 (50) ◽  
pp. 47608-47614 ◽  
Author(s):  
Guillaume Legrand ◽  
Sandrine Humez ◽  
Christian Slomianny ◽  
Etienne Dewailly ◽  
Fabien Vanden Abeele ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Growth Rate ◽  
Endoplasmic Reticulum ◽  
Growth Factor ◽  
Cell Growth ◽  
Intracellular Calcium ◽  
Lncap Cell ◽  
Fura 2 ◽  
Endoplasmic Reticulum Calcium ◽  
Calcium Pool

The present study demonstrates for the first time that intracellular calcium-ATPases and calcium pool content are closely associated with prostate cancer LNCaP cell growth. Cell growth was modulated by changing the amount of epidermal growth factor, serum, and androgene in culture media. Using the microspectrofluorimetric method with Fura-2 and Mag Fura-2 as probes, we show that in these cells, the growth rate is correlated with intracellular calcium pool content. Indeed, an increased growth rate is correlated with an increase in the calcium pool filling state, whereas growth-inhibited cells show a reduced calcium pool load. Using Western blotting and immunocytochemistry, we show that endoplasmic reticulum calcium pump expression is closely linked to LNCaP cell growth, and are a common target of physiological stimuli that control cell growth. Moreover, we clearly demonstrate that inhibition of these pumps, using thapsigargin, inhibits LNCaP cell growth and prevents growth factor from stimulating cell proliferation. Our results thus provide evidence for the essential role of functional endoplasmic reticulum calcium pumps and calcium pool in control of prostate cancer LNCaP cell growth, raising the prospect of new targets for the treatment of prostate cancer.

V2-like vasopressin receptor mobilizes intracellular Ca2+ in rat medullary collecting tubules

1993 ◽  
Vol 265 (1) ◽  
pp. F35-F45 ◽  
Author(s):  
A. Champigneulle ◽  
E. Siga ◽  
G. Vassent ◽  
M. Imbert-Teboul
Keyword(s):  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Free Calcium ◽  
Cytosolic Free Calcium ◽  
Free Calcium Concentration ◽  
Cytosolic Free Calcium Concentration ◽  
The Mean ◽  
V2 Antagonist ◽  
Collecting Tubules ◽  
Calcium Pool

Cytosolic free calcium concentration ([Ca2+]i) was measured in single microdissected rat medullary collecting tubules [outer (OMCD) and inner (IMCD)] to identify receptors involved in vasopressin (AVP)-induced [Ca2+]i increases. In both segments, [Phe2,Orn8]vasotocin ([Phe2,Orn8]VT), a specific V1 agonist, as well as the V2 agonist 1-desamino-8-D-AVP (dDAVP) triggered [Ca2+]i variations. In OMCD, the mean response to 10 nM AVP roughly corresponded to the sum of V1 and V2 agonists effects. In IMCD, dDAVP (10 nM) alone reproduced the calcium response to AVP (delta[Ca2+]i = 243 +/- 34 nM, n = 6, and 248 +/- 27 nM, n = 8, with dDAVP and AVP, respectively). Furthermore, in the same experiments V1 and V2 maximal effects were not additive ([Phe2,Orn8]VT = 154 +/- 21 nM, n = 6; dDAVP + [Phe2,Orn8]VT = 233 +/- 23 nM, n = 9). As AVP, dDAVP released intracellular calcium (delta[Ca2+]i in calcium-free medium = 182 +/- 24 nM, n = 8, vs. 182 +/- 14 nM, n = 6 with 10 nM dDAVP and AVP, respectively). Neither 8-(4-chlorophenyl-thio)-adenosine 3',5'-cyclic monophosphate nor forskolin modified [Ca2+]i. A cross-reaction of dDAVP with an oxytocin (OT) receptor can be excluded since 1) the specific OT agonist [Thr4,Gly7]OT (10 nM) increased only slightly [Ca2+]i (delta-[Ca2+]i = 20 +/- 5 nM, n = 11); 2) the dDAVP response was not altered by the specific OT antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid),2-(O-methyl)tyrosine,4-threonine, 8-ornithine,9-tyrosylamide]vasotocin [d(CH2)5(1),O-Me-Tyr2,Thr4,Tyr-NH2(9)]OVT; 3) it was insensitive to V1 antagonists but was totally blocked by the V1/V2 antagonist [d(CH2)5(1),O-Et-Tyr2,Val4]AVP ([delta[Ca2+]i = 18 +/- 4 nM, n = 6). These results indicate that in IMCD AVP increases [Ca2+]i via both V1 and V2 receptors. [Ca2+]i variations due to V2 receptors involve a mechanism independent of adenylate cyclase and coupled to the same intracellular calcium pool as V1 and V2 receptors.

Vitamin-D3 derivatives and breast-tumor cell growth: Effect on intracellular calcium and apoptosis

1995 ◽  
Vol 61 (6) ◽  
pp. 806-811 ◽  
Author(s):  
Brigitte Vandewalle ◽  
Louis Hornez ◽  
Nicole Wattez ◽  
Françoise Revillion ◽  
Jean Lefebvre
Keyword(s):  
Cell Growth ◽  
Tumor Cell ◽  
Intracellular Calcium ◽  
Vitamin D3 ◽  
Breast Tumor ◽  
Growth Effect ◽  
Tumor Cell Growth ◽  
Breast Tumor Cell

Effect of exracellular ATP on breast tumor cell growth, implication of intracellular calcium

1994 ◽  
Vol 85 (1) ◽  
pp. 47-54 ◽  
Author(s):  
B. Vandewalle ◽  
L. Hornez ◽  
F. Revillion ◽  
J. Lefebvre
Keyword(s):  
Cell Growth ◽  
Tumor Cell ◽  
Intracellular Calcium ◽  
Breast Tumor ◽  
Tumor Cell Growth ◽  
Breast Tumor Cell

Agonist interactions at the calcium pools in skinned and unskinned canine tracheal smooth muscle

1987 ◽  
Vol 65 (8) ◽  
pp. 1780-1787 ◽  
Author(s):  
M. S. Kannan ◽  
C. Davis ◽  
A. R. C. Ladenius ◽  
L. Kannan
Keyword(s):  
Smooth Muscle ◽  
Intracellular Calcium ◽  
Calcium Release ◽  
Rank Order ◽  
Calcium Sensitivity ◽  
Tracheal Smooth Muscle ◽  
Muscle Fibres ◽  
High Calcium ◽  
Calcium Sources ◽  
Calcium Pool

We studied the functionally discrete calcium sources used by acetylcholine, 5-hydroxytryptamine, histamine and high K+ in the dog tracheal smooth muscle. The extracellular calcium dependence of their responses was assessed by altering the calcium and by pretreatment with the calcium antagonist, nifedipine. The intracellular calcium pool was assessed by studying the interactions between caffeine and the agonists in both skinned and unskinned preparations. The extent of overlap for the different calcium pools between the various agonists was determined by studying the dose–response relationships of these agents before and after pretreatment with another agonist, i.e., the conditioning agonist, in zero calcium conditions. The rank order of sensitivity to calcium removal and to nifedipine was histamine > KCl > 5-hydroxytryptamine > acetylcholine. Caffeine-induced atenuation of the agonist responses was predominantly through physiological antagonism. However, the caffeine responses in unskinned fibres were augmented by pretreatment with the agonists through both nifedipine-sensitive (as with KCl) and -insensitive (as with acetylcholine) mechanisms. The responses to acetylcholine and caffeine were inhibited by theophylline and forskolin. In the skinned muscle fibres, the pCa–tension relationship suggested high calcium sensitivity, a significant caffeine-sensitive calcium pool, and no evidence of calcium release by exogenous inositol trisphosphate. The results are consistent with multiple extracellular and intracellular calcium sources for the agonist responses. We observed considerable overlap of the calcium sources used by these agonists. Of the four agonists studied, histamine appeared to inhibit the release and sequestration of calcium utilized by the other agonists most effectively.

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