Gastric mucosal cell proliferation during development in rats and effects of pentagastrin

1982 ◽  
Vol 242 (2) ◽  
pp. G135-G139 ◽  
Author(s):  
A. P. Majumdar ◽  
L. R. Johnson
Keyword(s):  
Cell Proliferation ◽  
Dna Synthesis ◽  
Thymidine Kinase ◽  
Kinase Activity ◽  
Cell Loss ◽  
Saline Control ◽  
Mucosal Cell ◽  
Thymidine Kinase Activity ◽  
Old Rats

Changes in cell proliferation and cell loss in the gastric mucosa were examined during the first 4 wk of life. The effect of pentagastrin on these parameters before and after weaning was also investigated. The results revealed that DNA content of mucosa and lumen increased with age. However, when luminal DNA (an assessment of cell loss) content was expressed as percent of total mucosal DNA (referred to as percent cell loss), an inverse relationship with age was observed. The rate of mucosal DNA synthesis, measured in vitro, was found to remain elevated up to the age of 15 days and then dropped dramatically within the next 5--6 days after which it decreased slowly. The rate of mucosal DNA synthesis in 5- to 15-day-old rats was found to be 10--15 times higher than in 20- to 30-day-old rats. In 10-day-old suckling young, mucosal thymidine kinase activity was also found to be higher than in 20- to 28-day-old rats. On the other hand, total incorporation of [3H]thymidine into mucosal DNA per stomach was found to be significantly greater in 21- to 28-day-old weaned rats than in the 10-day-old suckling young. Multiple injections of pentagastrin to 28-day-old rats significantly increased mucosal DNA synthesis and thymidine kinase activity by 43 and 200%, respectively, and cell loss by 30% when compared with the saline control. The hormone did not affect DNA synthesis, thymidine kinase, or cell loss in 10-day-old rats. There were considerable increases in 20-day-old rats that were not statistically significant due to the variation of the data.

ANF-C-receptor-mediated inhibition of aortic smooth muscle cell proliferation and thymidine kinase activity

1994 ◽  
Vol 266 (1) ◽  
pp. R194-R203 ◽  
Author(s):  
P. A. Cahill ◽  
A. Hassid
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Dna Synthesis ◽  
Thymidine Kinase ◽  
Receptor Binding ◽  
Kinase Activity ◽  
Thymidine Kinase Activity ◽  
Aortic Smooth Muscle ◽  
Inhibition Of Dna Synthesis ◽  
Type Receptor

We have investigated the inhibition of DNA synthesis and cell proliferation by rat atrial natriuretic factor [rANF-(99-126)] and several synthetic peptides that bind selectively to the ANF-C-type clearance receptors in subcultured aortic smooth muscle cells. These peptides decreased serum-induced 1) [3H]thymidine incorporation, 2) cell proliferation, and 3) thymidine kinase activity without altering basal or elevated cAMP or cGMP levels. In contrast, another ANF-C-receptor-binding peptide, des[Gln116,Ser117,Gly118,Leu119,Gly120] rANF-(102-121)-NH2 (cANF), failed to decrease serum-induced mitogenesis, yet 100 nM cANF reversed the inhibition of DNA synthesis and cell proliferation and the decrease of thymidine kinase activity elicited by other C receptor-binding peptides, including rANF-(99-126), rANF-(103-125), and porcine C-type natriuretic peptide [pCNP-(1-22)]. Delayed addition experiments indicated that atrial peptides influence a relatively late event (or events) during the G1 phase of the cell cycle. The inhibition of DNA synthesis by C-receptor-binding atrial peptides appeared to be selective for aortic smooth muscle cells, inasmuch as a potent inhibitory agonist peptide, Cys116-rANF-(102-116), was without significant influence on the incorporation of thymidine in cultured rat mesangial cells or bovine pulmonary artery endothelial cells. These results indicate that atrial natriuretic peptide analogues decrease vascular smooth muscle cell mitogenesis and proliferation by a cyclic nucleotide-independent mechanism involving the C-type receptor. Moreover the inhibition of DNA synthesis by rANF-(99-126) and the neuropeptide pCNP-(1-22) appears to be mediated by the ANF-C-type receptor and is associated with inhibition of thymidine kinase activity.

Thymidine kinase, thymidylate synthase, and endothelial cell growth under hyperoxia

1987 ◽  
Vol 62 (1) ◽  
pp. 10-14 ◽  
Author(s):  
A. F. Junod ◽  
H. Petersen ◽  
L. Jornot
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Dna Synthesis ◽  
Thymidine Kinase ◽  
Thymidylate Synthase ◽  
Kinase Activity ◽  
Primary Cultures ◽  
Thymidine Kinase Activity ◽  
Aortic Endothelial Cells ◽  
Key Enzyme

To determine the respective role of thymidine kinase and thymidylate synthase activities in the hyperoxia-induced decrease in DNA synthesis and their relationship with cell replication, we measured these two enzyme activities in primary cultures of porcine aortic endothelial cells under different O2 concentrations for various durations. In confluent cells, exposure to 95% O2 for 5 days reduced thymidine kinase activity to 15% of control values; thymidylate synthase activity was unaffected. In preconfluent cells exposed to 95% O2 for 2 days, similar results were obtained, together with evidence for arrest in cell proliferation. Thymidylate synthase activity could therefore not be related to decreased cell proliferation under hyperoxia. [3H]thymidine incorporation into DNA, thymidine kinase activity, and cell proliferation were all similarly affected under exposure to graded O2 concentration for 2 days. Thymidine kinase appears to be a key enzyme in the modulation of DNA synthesis from thymidine and in its replication in endothelial cells.

Aging: altered responsiveness of gastric mucosa to epidermal growth factor

1989 ◽  
Vol 257 (4) ◽  
pp. G554-G560 ◽  
Author(s):  
A. P. Majumdar ◽  
F. L. Arlow
Keyword(s):  
Growth Factor ◽  
Gastric Mucosa ◽  
Epidermal Growth Factor ◽  
Dna Synthesis ◽  
Thymidine Kinase ◽  
Membrane Fraction ◽  
Kinase Activity ◽  
Thymidine Kinase Activity ◽  
Epidermal Growth ◽  
K Activity

The present investigation examines the responsiveness of the gastric mucosa to the growth-promoting action of epidermal growth factor (EGF) during advancing age. Two sets of experiments were performed. In the first set of experiments, groups of 4-, 8-, 16-, and 24-mo-old Fischer 344 rats were injected subcutaneously at 12-h intervals for 2 days with either EGF (10 micrograms/kg) in gelatin or the vehicle only (controls). The animals were killed 16-18 h after the last injection. The oxyntic gland mucosa was assayed for thymidine kinase and the rate of DNA synthesis in vitro (indicators of proliferative activity) as well as for tyrosine kinase (Tyr-k) activity. In control rats, the rate of DNA synthesis and thymidine kinase activity rose steadily between 4 and 24 mo of age. However, whereas Tyr-k activity in the gastric mucosal cytosol changed only marginally with age, activity of the enzyme in the membrane fraction rose steadily between 4 and 16 mo and then increased abruptly. EGF stimulated gastric mucosal DNA synthesis and thymidine kinase activity in 4- to 16-mo-old rats compared with the corresponding controls, but in the 24-mo-old animals, it caused a significant 40-50% inhibition. EGF had no demonstrable effect on Tyr-k activity in either cytosolic or membrane fraction. We postulated that Tyr-k activity might have returned to basal level 16-18 h after the last EGF injection.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Induction of thymidine kinase activity and clonal growth of certain leukemic cell lines by a granulocyte-derived factor

Blood ◽  
1990 ◽  
Vol 75 (12) ◽  
pp. 2438-2444 ◽  
Author(s):  
CK Ho ◽  
BR Ou ◽  
ML Hsu ◽  
SN Su ◽  
CH Yung ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Dna Synthesis ◽  
Thymidine Kinase ◽  
Cell Lines ◽  
Kinase Activity ◽  
Leukemic Cell ◽  
Metabolic Inhibitors ◽  
Dependent Manner ◽  
Thymidine Kinase Activity ◽  
Leukemic Cell Lines

Abstract Normal polymorphonuclear neutrophils (PMNs) constitutively secrete a mediator designated granulocyte-derived factor (GDF) that can enhance the uptake of 3H-thymidine (3- to 20-fold) by the molt-3, CTV-1, and K562 leukemic cell lines in a dose-dependent manner. GDF is heat labile (56 degrees C for 30 minutes) and acid labile (pH 2.0) and is sensitive to treatment with bacterial protease type IV. Our preliminary studies suggest that GDF is non-dialyzable (molecular weight cutoff, 12,000), binds to diethylaminoethyl (DEAE), and has an apparent molecular weight (mol wt) of about 40 Kd. Production of GDF is unaffected by treatment of PMN with activating agents (interferon gamma, OK432, phorbol ester, calcium ionophore, poly I:C) or metabolic inhibitors (actinomycin-D and cyclohexamide), suggesting that GDF is constitutively secreted. Despite the marked enhancement of 3H-thymidine uptake, cell number and the rate of DNA synthesis in GDF responsive cultures remain unchanged. In contrast, the clonogenic efficiency of the responsive cells is greatly increased in the presence of GDF. These phenomena occur in parallel to an amplification of the level of thymidine kinase activity in the sensitive cells. GDF is distinct from a panel of different lymphokines and monokines in antigenicity and biochemical and functional characteristics, and is possibly a novel cytokine that can alter the pattern of DNA synthesis and growth characteristics of certain hematopoietic cells. However, its biologic and physiologic significance remains to be determined.

Mutant strains of Tetrahymena thermophila defective in thymidine kinase activity: biochemical and genetic characterization

1982 ◽  
Vol 2 (8) ◽  
pp. 930-938
Author(s):  
K V Cornish ◽  
R E Pearlman
Keyword(s):  
Thymidine Kinase ◽  
Kinase Activity ◽  
Tetrahymena Thermophila ◽  
Permissive Temperature ◽  
Thymidine Kinase Activity ◽  
Cell Extracts ◽  
Mutant Strains ◽  
Nucleoside Phosphotransferase

Three mutant strains, one conditional, of Tetrahymena thermophila were defective in thymidine phosphorylating activity in vivo and in thymidine kinase activity in vitro. Nucleoside phosphotransferase activity in mutant cell extracts approached wild-type levels, suggesting that thymidine kinase is responsible for most, if not all, thymidine phosphorylation in vivo. Thymidine kinase activity in extracts of the conditional mutant strain was deficient when the cells were grown or assayed or both at the permissive temperature, implying a structural enzyme defect. Analysis of the reaction products from in vitro assays with partially purified enzymes showed that phosphorylation by thymidine kinase and nucleoside phosphotransferase occurred at the 5' position. Genetic analyses showed that the mutant phenotype was recessive and that mutations in each of the three mutant strains did not complement, suggesting allelism.

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