STIMULATION OF DNA SYNTHESIS IN RAT LIVER BY ADRENALECTOMY

1974 ◽  
Vol 60 (2) ◽  
pp. 315-319 ◽  
Author(s):  
LUCIA DESSER-WIEST

SUMMARY The following effects were observed in the liver of male rats in the first few days after adrenalectomy: the rate of thymidine incorporation into DNA was increased three- to fourfold in the 2 days after adrenalectomy. The mitotic index was increased 5·5-fold on the first day and 15-fold on the second day after the operation. The number of tetraploid cells rose from 40 to 68%. While the subsequent administration of cortisol, cortisone or corticosterone to the adrenalectomized animals reduced DNA synthesis to the normal level, testosterone and oestrone were without effect. It is suggested that liver growth is regulated by the concentration of corticosteroids in the blood.

1982 ◽  
Vol 65 (3) ◽  
pp. 478-480 ◽  
Author(s):  
G.M. Ledda ◽  
A. Columbano ◽  
T. Perra ◽  
P. Pani

1983 ◽  
Vol 244 (5) ◽  
pp. G469-G474 ◽  
Author(s):  
J. P. Buts ◽  
R. De Meyer ◽  
J. Kolanowski

This study was undertaken to determine whether the rat colon exhibits ontogenic changes in epithelial cell proliferation and DNA synthesis during growth. DNA synthesis was measured at intervals after birth in four colonic segments by the incorporation rates of [3H]thymidine. The labeled crypt cell index was determined by radioautography. New findings from our study are that 1) in each colonic segment of suckling rats, [3H]thymidine incorporation rate overshot the adult levels (49-119%) with a peak occurring at day 14 postpartum, 2) between days 14 and 20, the incorporation rates declined sharply to adult values and remained thereafter unchanged until adulthood; during the same period, the labeled and mitotic index decreased, respectively, from 52 to 19% and from 3.58 to 1.43%, 3) the decrease in DNA synthesis and in cell proliferation rates was concomitant with an upsurge in plasma total corticosterone initiated on day 14, and 4) treatment of 10-day-old sucklings with physiological doses of hydrocortisone for 4 consecutive days significantly depressed (P less than 0.01) colonic DNA content and DNA synthesis rates to levels about 45-67% of the control values. These data indicate that growth of the colon may be under the control of glucocorticoid secretion at the weaning period.


Blood ◽  
1999 ◽  
Vol 94 (1) ◽  
pp. 114-126 ◽  
Author(s):  
Michael Haslauer ◽  
Kurt Baltensperger ◽  
Hartmut Porzig

Proliferation, differentiation, and survival of erythroid progenitor cells are mainly regulated by stem cell factor (SCF) and erythropoietin (Epo). Using normal human progenitors, we analyzed the role of Ca2+-sensitive protein kinase C (PKC) subtypes and of G-protein–coupled receptor ligands on growth factor–dependent DNA synthesis. We show that stimulation of DNA synthesis by the two growth factors requires activation of PKC. Inhibitors of Ca2+-activated PKC subtypes blocked the growth factor–induced 3H-thymidine incorporation. SCF and Epo caused no significant translocation of PKC into the membrane, but treatment of intact cells with either of the two cytokines resulted in enhanced activity of immunoprecipitated cytosolic PKC. Stimulation of PKC with the phorbol ester PMA mimicked the cytokine effect on DNA synthesis. Epo-, SCF-, and PMA-induced thymidine incorporation was potently inhibited by thrombin (half-maximal inhibition with 0.1 U/mL). This effect was mediated via the G-protein-coupled thrombin receptor and the Rho guanosine triphosphatase. Adenosine diphosphate caused a modest Ca2+-dependent stimulation of DNA synthesis in the absence of cytokines and specifically enhanced the effect of SCF. Cyclic 3′,5′-adenosine monophosphate exerted a selective inhibitory effect on Epo-stimulated thymidine incorporation. Our results define PKC as major intermediate effector of cytokine signaling and suggest a role for thrombin in controlling erythroid progenitor proliferation.


1984 ◽  
Vol 12 (1) ◽  
pp. 106-111 ◽  
Author(s):  
Werner K. Lutz ◽  
Marie-Therese Büsser ◽  
Peter Sagelsdorff

1996 ◽  
Vol 6 (2) ◽  
pp. 92-98 ◽  
Author(s):  
R GARCIACANERO ◽  
J DEDIEGO ◽  
C TRILLA ◽  
M DEFORONDA ◽  
J DIAZGIL ◽  
...  

1984 ◽  
Vol 74 (3) ◽  
pp. 337-344 ◽  
Author(s):  
Shoji Nishiyama ◽  
Kenichi Nakamura

1982 ◽  
Vol 30 (7) ◽  
pp. 677-681 ◽  
Author(s):  
J M Jacobi ◽  
H M Lloyd ◽  
J D Meares

Nuclear diameter, DNA synthesis, and mitotic index in the pituitary cells of male rats and serum prolactin were measured after a period of 8 days of treatment with a dopamine agonist and an antagonist given with and without estrogen. In the absence of estrogen, the dopamine agonist, bromocriptine, diminished the mean nuclear diameter of the pituitary cells and lowered pituitary DNA synthesis, and the dopamine-blocking agent haloperidol had no effect. Estrogen increased the mean nuclear diameter, pituitary mitotic index, and DNA synthesis. Bromocriptine prevented the estrogen-induced increase in mean nuclear diameter and pituitary DNA synthesis and mitotic index were lowered. Haloperidol augmented the estrogen-induced increase in mean nuclear diameter, pituitary DNA synthesis, and mitotic index. Positive correlations were obtained between mean nuclear diameter and DNA synthesis and serum prolactin. It was concluded that nuclear diameter was influenced by both DNA synthesis and secretory activity in pituitary cells.


1997 ◽  
Vol 272 (3) ◽  
pp. H1470-H1479 ◽  
Author(s):  
M. F. Ethier ◽  
J. G. Dobson

We investigated adenosine stimulation of DNA synthesis in human endothelial cells by measuring [3H]thymidine incorporation in cultures derived from human umbilical veins. After 18 h of exposure to adenosine in serum-free medium, endothelial cell [3H]thymidine incorporation was increased by 30-64%. Adenosine-induced DNA synthesis was not mimicked by adenosine receptor agonists and was not inhibited by adenosine receptor antagonists. Adenosine-induced DNA synthesis was inhibited 81% by 100 microM 5'-(N,N-dimethyl)amiloride, an inhibitor of Na+/H+ exchange, and was totally inhibited by 10 microM 2',4'-dibromoacetophenone, an inhibitor of phospholipase A2 (PLA2). Adenosine increased adenosine 3',5'-cyclic monophosphate levels in endothelial cells, but adenosine-induced DNA synthesis was not inhibited by the protein kinase A (PKA) inhibitor Rp-cAMPS. Both ATP and the phorbol ester 4beta-phorbol 12-myristate 13-acetate (PMA) increased DNA synthesis in human endothelial cells. Stimulation by ATP was inhibited by the P2-receptor antagonist suramin, and PMA stimulation was inhibited by the protein kinase C (PKC) inhibitor H-7. Neither suramin nor H-7 inhibited adenosine-stimulated DNA synthesis. The results suggest that Na+/H+ exchange and PLA2 are involved in adenosine-induced DNA synthesis in cultures of human endothelial cells independently of adenosine receptor, PKA, or PKC activation.


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