An analysis of proliferative activity in innervated and denervated forelimb regenerates of the newt, Notophthalmus viridescens

Development ◽  
1987 ◽  
Vol 100 (4) ◽  
pp. 619-628 ◽  
Author(s):  
D.J. Goldhamer ◽  
R.A. Tassava
Keyword(s):  
Cell Cycle ◽  
Mitotic Index ◽  
Proliferative Activity ◽  
Thymidine Incorporation ◽  
Labelling Index ◽  
Notophthalmus Viridescens ◽  
Pulse Labelling ◽  
Adult Newt ◽  
Kinetics Of ◽  
Continuous Labelling

Pulse and continuous labelling with [3H]thymidine combined with mitotic index determinations provided data on the kinetics of cell cycling in innervated and denervated early and mid-bud forelimb blastemas of the adult newt, Notophthalmus viridescens. Most or all blastema cells cycle during regeneration and are thus part of the proliferative fraction. At any given moment, however, only 26% of the blastema cells are actively progressing through the cell cycle, with the remainder being in a state of transient quiescence (TQ). The small size of the actively cycling (AC) population may in part explain the relatively slow rate of regeneration exhibited by the adult newt. The pulse-labelling index and mitotic index of denervated blastemas paralleled control values for 48h following nerve withdrawal, but both parameters were significantly reduced by 72h. By 5 days postdenervation, cell cycle activity was essentially zero. The combined pulse and continuous labelling data suggest that nerves may be primarily involved in the entry of TQ cells into the AC population, with subsequent progression through the cell cycle being less dependent on innervation. Relative to controls, no early postdenervation increases in TCA-precipitable [3H]thymidine incorporation, pulse-labelling index or mitotic index were observed.

Neurotrophic control of events in injured forelimbs of larval urodeles

Development ◽  
1982 ◽  
Vol 69 (1) ◽  
pp. 183-192
Author(s):  
Anthony L. Mescher
Keyword(s):  
Cell Cycle ◽  
Dna Synthesis ◽  
Mitotic Activity ◽  
Mitotic Index ◽  
Elevated Level ◽  
Labelling Index ◽  
Neurotrophic Control ◽  
Epimorphic Regeneration ◽  
Baseline Levels

Denervated forelimbs and contralateral innervated forelimbs of Ambystoma larvae were injured internally distal to the elbow by compression with watchmaker's forceps. Innervated controls completely repaired the crush injury within one week; denervated limbs failed to repair the injury and exhibited varying degrees of limb regression. Histological examination revealed that the process of tissue dedifferentiation initiated by injury was more extensive in denervated, regressing limbs than in controls. In innervated limbs, both the DNA labelling index and the mitotic index peaked approximately 4–6 days after the injury and returned to baseline levels by 10 days. In denervated limbs, the DNA labelling index also increased and remained at an elevated level for at least 2 weeks after the injury, but significant mitotic activity was not observed. The data indicate that intact nerves are not needed for cellular dedifferentiation, cell cycle re-entry, and DNA synthesis in injured limbs, but are required for the cells to proliferate and repair the injury. These results are discussed together with those of similar experiments on the role of nerves during the initiation of epimorphic regeneration in amputated limbs.

EFFECT OF DEXAMETHASONE ON CELL POPULATION KINETICS IN THE ADRENAL CORTEX OF THE PREPUBERTAL MALE RAT

1974 ◽  
Vol 62 (3) ◽  
pp. 527-536 ◽  
Author(s):  
N. A. WRIGHT ◽  
D. R. APPLETON ◽  
A. R. MORLEY
Keyword(s):  
Cell Cycle ◽  
Latent Period ◽  
Adrenal Cortex ◽  
Direct Action ◽  
Tritiated Thymidine ◽  
Labelling Index ◽  
Male Rats ◽  
Male Rat ◽  
Rate Of Increase ◽  
Continuous Labelling

SUMMARY The effect of a single injection of dexamethasone on adrenocortical cell proliferation was studied in prepubertal male rats using tritiated thymidine. After a short latent period, all zones of the adrenal cortex showed a rapid decrease in both labelling and mitotic indices. After a prolonged period when very low indices were apparent, there was a rapid rise in both proliferative indices with most zones showing a considerable increase above control values. A more detailed study of the initial depression showed that after a latent period of about 5 h the labelling index fell approximately 8 h before the mitotic index. This differential response in the labelling and mitotic indices was consistent with a block in the cell cycle late in the pre-DNA synthetic interval of the cell cycle (G1), with cells being prevented from entering DNA synthesis. This hypothesis was also supported by an experiment involving continuous labelling of control and dexamethasone-treated animals; again after a latent period of 5–6 h, the rate of increase of the continuous labelling index fell as cells became blocked in late G1. By analogy with other tissues, results are interpreted in terms of a direct action of dexamethasone on adrenocortical cells; this steroid-sensitive step in the cell cycle may be important in the control of growth in the adrenal cortex.

scholarly journals An autoradiographic study of cellular proliferaton, DNA synthesis and cell cycle variability in the rat liver caused by phenobarbital-induced oxidative stress: The protective role of melatonin

2007 ◽  
Vol 12 (3) ◽  
Author(s):  
Gamal El-Sokkary
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Lipid Peroxidation ◽  
Dna Synthesis ◽  
Rat Liver ◽  
Cycle Time ◽  
Proliferative Activity ◽  
Labelling Index ◽  
Male Rats ◽  
Cell Cycle Time

AbstractThe protective effect of melatonin against phenobarbital-induced oxidative stress in the rat liver was measured based on lipid peroxidation levels (malondialedyde and 4-hydroxyalkenals). Cellular proliferation, DNA synthesis and cell cycle duration were quantitated by the incorporation of 3H-thymidine, detected by autoradiography, into newly synthesized DNA. Two experiments were carried out in this study, each on four equal-sized groups of male rats (control, melatonin [10 mg/kg], phenobabital [20 mg/kg] and phenobarbital plus melatonin). Experiment I was designed to study the proliferative activity and rate of DNA synthesis, and measure the levels of lipid peroxidation, while experiment II was for cell cycle time determination. Relative to the controls, the phenobarbital-treated rats showed a significant increase (P < 0.01) in the lipid peroxidation levels (30.7%), labelling index (69.4%) and rate of DNA synthesis (37.8%), and a decrease in the cell cycle time. Administering melatonin to the phenobarbital-treated rats significantly reduced (P < 0.01) the lipid peroxidation levels (23.5%), labelling index (38.2%) and rate of DNA synthesis (29.0%), and increased the cell cycle time. These results seem to indicate that the stimulatory effect of phenobarbital on the oxidized lipids, proliferative activity, kinetics of DNA synthesis and cell cycle time alteration in the liver may be one of the mechanisms by which the non-genotoxic mitogen induces its carcinogenic action. Furthermore, melatonin displayed powerful protection against the toxic effect of phenobarbital.

scholarly journals Expression of the c-myc proto-oncogene in multiple myeloma and chronic lymphocytic leukemia: an in situ analysis

Blood ◽  
1991 ◽  
Vol 78 (1) ◽  
pp. 180-191 ◽  
Author(s):  
R Greil ◽  
B Fasching ◽  
P Loidl ◽  
H Huber
Keyword(s):  
Cell Cycle ◽  
Multiple Myeloma ◽  
Chronic Lymphocytic Leukemia ◽  
Peripheral Blood ◽  
Proliferative Activity ◽  
Plasma Cells ◽  
Lymphocytic Leukemia ◽  
Myc Gene ◽  
Gene Transcripts

Abstract The c-myc gene plays a pivotal role in mediating the competence state for cell cycle transversion. This biologic role is in contradiction to reports of elevated expression of the gene in multiple myeloma, a tumor with restricted self-renewal capacity. To more clearly define the role of this gene in plasma cells of myeloma patients, c-myc messenger RNA (mRNA) and/or oncoprotein expression were semiquantitatively analyzed on the single cell level in 19 cases of multiple myeloma, among them 1 biclonal case and 1 case with coexistent chronic lymphocytic leukemia (CLL). Performing anti-sense/mRNA in situ hybridization, mature c-myc gene transcripts were detected in 92% (12 of 13) of cases and could definitely be attributed to the plasma cells by our study. The number of Ki 67-positive plasma cells actively passing the cell cycle was less than 1% and independent of c-myc gene expression. However, because the presence of the 152-c-MYC epitope was correlated to extent of marrow plasmacytosis (r = .64; P = .043) and content of plasmablasts (P = .09), the c-myc gene might serve a function different from proliferative activity, but also associated with tumor cell mass. In CLL cells (21 of 22 cases) and their benign counterparts, ie, bone marrow and peripheral blood lymphocytes, the anti-sense/c-myc mRNA hybridization signals remained below the threshold considered as cutpoint between negative and positive. The low amounts of c-myc transcripts were correlated to neither stage of disease (P = .52) nor lymphocyte counts (P = .24). Because the numbers of peripheral blood lymphoma cells were independent of tumor mass and of c-myc gene transcripts expressed, peripheral blood lymphocytosis might more likely reflect homing processes than proliferative activity in CLL.

Sign in / Sign up

Export Citation Format

Share Document