scholarly journals Ribonucleic acid labelling and nucleotide pools during compensatory renal hypertrophy

1974 ◽  
Vol 144 (3) ◽  
pp. 447-453 ◽  
Author(s):  
J M Hill ◽  
G Ab ◽  
R A Malt
Keyword(s):  
Rna Synthesis ◽  
Single Injection ◽  
Specific Radioactivity ◽  
Compensatory Hypertrophy ◽  
Rrna Synthesis ◽  
Renal Hypertrophy ◽  
Rna Content ◽  
Compensatory Renal Hypertrophy ◽  
Precursor Rna ◽  
Ribosomal Precursor

During the first 48h of compensatory renal hypertrophy induced by unilateral nephrectomy, RNA content per cell increased by 20–40%. During this period, rates of RNA synthesis derived from the rates of labelling of UTP and RNA after a single injection of [5-3H]uridine showed no change in the rate of RNA synthesis (3.1nmol of UTP incorporated into RNA/min per mg of RNA). ATP and ADP pools were not changed. The rate of RNA synthesis was considerably in excess of the increment of total RNA appearing in the kidneys. With [5-3H]uridine as label, only continuous infusion for 24h could produce an increase (60%) in the specific radioactivity of renal rRNA in mice with contralateral nephrectomies. With a single injection of [methyl-3H]methionine used to identify methyl groups inserted into newly synthesized rRNA, the specific radioactivity of this rRNA was unchanged 5h after contralateral nephrectomy, increased by 60% at 9–48h, and returned to normal values at 120h. Most RNA synthesized in both nephrectomized and sham-nephrectomized mice has a short half-life. Since total cellular RNA content increases in compensatory hypertrophy despite unchanged rates of rRNA synthesis, the accretion of RNA might involve conservation of ribosomal precursor RNA or a change in rate of degradation of mature rRNA.

Regulation of ribosome synthesis during compensatory renal hypertrophy in mice

1987 ◽  
Vol 253 (4) ◽  
pp. C506-C513 ◽  
Author(s):  
A. J. Ouellette ◽  
R. Moonka ◽  
A. D. Zelenetz ◽  
R. A. Malt
Keyword(s):  
Ribosomal Protein ◽  
Ribosomal Proteins ◽  
Rdna Transcription ◽  
Renal Hypertrophy ◽  
Renal Growth ◽  
Compensatory Renal Hypertrophy ◽  
Steady State Levels ◽  
Precursor Rna ◽  
Ribosomal Precursor

Ribosomal synthesis was studied at the transcriptional and translational levels to investigate the mechanisms of ribosome accretion during compensatory renal hypertrophy. As measured by in vitro transcriptional runoff comparisons 6-48 h after surgery, nuclei from the kidney remaining after contralateral nephrectomy show an increase of up to 150% in the rate of synthesis of ribosomal precursor RNA. The rate of rDNA transcription is 40-50% greater than control values as early as 6 h after nephrectomy; by 48 h, the rate returns to normal. In contrast to the stimulated transcription of rDNA and accretion of rRNA, the steady-state levels and the cytoplasmic distribution of ribosomal protein mRNAs S16 and L10 remain unchanged during induced renal growth. Thus coordinate production of adequate protein for increased assembly of ribosomes during induced renal growth appears to be accomplished by increasingly efficient translation of existing ribosomal protein mRNAs or by post-translational stabilization of ribosomal proteins. The rate of rDNA transcription may be regulated by accelerating the transcription of already functioning genes or, more likely, by recruiting transcription units that are transcriptionally inactive in the normal kidney.

scholarly journals Conservation of ribosomal RNA during compensatory renal hypertrophy. A major mechanism in RNA accretion.

1976 ◽  
Vol 69 (3) ◽  
pp. 548-556 ◽  
Author(s):  
W T Melvin ◽  
A Kumar ◽  
R A Malt
Keyword(s):  
Ribosomal Rna ◽  
Cultured Cells ◽  
Compensatory Hypertrophy ◽  
Mouse Kidney ◽  
Average Increase ◽  
Renal Hypertrophy ◽  
Major Mechanism ◽  
Compensatory Renal Hypertrophy

After removal of one mouse kidney, compensatory hypertrophy in the remaining kidney is marked in 2 days by a 20% average increase in ribosomal RNA (rRNA) per cell. Both 28S and 18S RNA are conserved during the initial stages of compensatory renal hypertrophy to an extent sufficient to account for the rest of the observed accumulation of rRNA. Like some cultured cells, the kidney conserves rRNA during physiological growth.

scholarly journals THE DEGREE OF COMPENSATORY RENAL HYPERTROPHY FOLLOWING UNILATERAL NEPHRECTOMY

1938 ◽  
Vol 67 (4) ◽  
pp. 515-519 ◽  
Author(s):  
Lois L. MacKay ◽  
T. Addis ◽  
Eaton M. MacKay
Keyword(s):  
Protein Intake ◽  
Compensatory Hypertrophy ◽  
Unilateral Nephrectomy ◽  
Albino Rats ◽  
Renal Hypertrophy ◽  
Young Rats ◽  
Compensatory Renal Hypertrophy ◽  
Old Rats

Compensatory hypertrophy of the kidney in albino rats is increased by an increase in the protein intake. The effect is greater in old rats than young rats. Successive increases in the protein intake are followed by a reduction in the increase in the degree of compensatory renal hypertrophy.

scholarly journals NUCLEAR ENVELOPE-ASSOCIATED RESUMPTION OF RNA SYNTHESIS IN LATE MITOSIS OF HELA CELLS

1973 ◽  
Vol 59 (1) ◽  
pp. 150-164 ◽  
Author(s):  
T. Simmons ◽  
P. Heywood ◽  
L. Hodge
Keyword(s):  
Protein Synthesis ◽  
Nuclear Envelope ◽  
Rna Synthesis ◽  
Electron Microscope Autoradiography ◽  
Molecular Synthesis ◽  
Hela S3 ◽  
Precursor Rna ◽  
Ribosomal Precursor ◽  
Hela S3 Cells ◽  
Silver Grains

The restitution of RNA synthesis in cultures progressing from metaphase into interphase (G1) has been investigated in synchronized HeLa S3 cells by using inhibitors of macro-molecular synthesis and the technique of electron microscope autoradiography. The rate of incorporation of radioactive uridine into RNA approached interphase levels in the absence of renewed protein synthesis. In contrast, maintenance of this rate in G1 was dependent upon renewed protein synthesis. Restoration of synthesis of heterogeneous nuclear RNA occurred under conditions that inhibited production of ribosomal precursor RNA. In autoradiographs of individual cells exposed to radioactive uridine, silver grains were first detected after nuclear envelope reformation at the periphery of the chromosome mass but before chromosomal decondensation. These data are consistent with the following interpretation. Multiple RNA polymerase activities persist through mitosis and are involved in the initiation of RNA synthesis in early telophase at sites on the nuclear envelope.

Compensatory renal hypertrophy. I. Evidence for a factor of renal origin inhibiting DNA synthesis

1977 ◽  
Vol 55 (4) ◽  
pp. 839-847 ◽  
Author(s):  
J. Martel-Pelletier ◽  
M. Bergeron
Keyword(s):  
Molecular Weight ◽  
Dna Synthesis ◽  
Specific Inhibitor ◽  
Inhibitory Effect ◽  
Compensatory Hypertrophy ◽  
Partial Purification ◽  
Dna Uptake ◽  
Renal Hypertrophy ◽  
Compensatory Renal Hypertrophy

This study describes a method for the measurement and partial purification of a factor seemingly involved in the regulation of the renal mass.After homogenization at 4 °C, rabbit kidneys were centrifuged for 100 min at 105 000 g. The resulting supernatant (S-105) was lyophilized and tested on kidney slices obtained from rats mononephrectomized 48 h previously. We have developed a method based on the inhibition of DNA synthesis to measure the activity of the S-105. Slices of renal cortex, undergoing compensatory hypertrophy, were incubated in vitro in Hanks' medium at 37 °C, pH 7.4, in an O2–CO2 atmosphere in the presence of 0.144 μg (20 μCi (1 Ci = 37 GBq)) [3H]thymidine.An inhibition of DNA uptake of [3H]thymidine was noted in the presence of S-105. When other media (Hanks', sucrose, water) were used to extract S-105, the same type of inhibition was noted even though the sucrose buffer seemed ideal for the preservation of the inhibitory factor. The inhibitory effect was still observed after dialysis of S-105 against membranes permitting exclusion of molecules with molecular weight smaller than about 4000 (such as electrolytes and tissue thymidine). This inhibition seems to be specific, since other tissues such as liver in regeneration and rat intestine were not influenced by the dialyzed renal S-105. The dialyzable fraction did contain some inhibitors, but they were not specific for the kidney since they also acted on the liver and the jejunum.Our results suggest the existence, in the normal nephron, of a specific inhibitor of thymidine incorporation into DNA of kidneys undergoing a compensatory hypertrophy. This renal factor has a molecular weight of over 5000.

scholarly journals Carcinogenesis and Cellular Injury. The effect of ethionine on ribonucleic acid synthesis in rat liver

1975 ◽  
Vol 150 (3) ◽  
pp. 335-344 ◽  
Author(s):  
P F Swann ◽  
A C Peacock ◽  
S Bunting
Keyword(s):  
Protein Synthesis ◽  
Rna Synthesis ◽  
Acid Synthesis ◽  
Female Rat ◽  
Concurrent Administration ◽  
Polyamine Synthesis ◽  
Rrna Maturation ◽  
Precursor Rna ◽  
Inhibitor Of Protein Synthesis ◽  
Ribosomal Precursor

1. By 1h after administration of ethionine to the female rat the appearance of newly synthesized 18SrRNA in the cytoplasm is completely inhibited. This is not caused by inhibition of RNA synthesis, for the synthesis of the large ribosomal precursor RNA (45S) and of tRNA continues. Cleavage of 45S RNA to 32S RNA also occurs, but there was no evidence for the accumulation of mature or immature rRNA in the nucleus. 2. The effect of ethionine on the maturation of rRNA was not mimicked by an inhibitor of protein synthesis (cycloheximide) or an inhibitor of polyamine synthesis [methylglyoxal bis(guanylhydrazone)]. 3. Unlike the ethionine-induced inhibition of protein synthesis, this effect was not prevented by concurrent administration of inosine. A similar effect could be induced in HeLa cells by incubation for 1h in a medium lacking methionine. The ATP concentration in these cells was normal. From these two observations it was concluded that the effect of etionine on rRNA maturation is not caused by an ethionine-induced lack of ATP. It is suggested that ethionine, by lowering the hepatic concentration of S-adenosylmethionine, prevents methylation of the ribosomal precursor. The methylation is essential for the correct maturation of the molecule; without methylation complete degradation occurs.

scholarly journals Action of dichlorobenzimidazole riboside on RNA synthesis in L-929 and HeLa cells.

1976 ◽  
Vol 69 (2) ◽  
pp. 229-240 ◽  
Author(s):  
I Tamm ◽  
R Hand ◽  
L A Caliguiri
Keyword(s):  
Hela Cells ◽  
Rna Synthesis ◽  
Dose Range ◽  
Inhibitory Effect ◽  
Mouse Fibroblast ◽  
L Cells ◽  
Uridine Uptake ◽  
High Concentrations ◽  
Precursor Rna ◽  
Ribosomal Precursor

5,6-Dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB) inhibits RNA synthesis in L-929 cells (mouse fibroblast line) and HeLa cells (human epitheloid carcinoma line) within 2 min of addition of the compound to the medium. By removing DRB from the medium, the inhibition is promptly and completely reversed after treatment of cells for as long as 1 h or even longer. The inhibitory effect of DRB on the overall rate of RNA synthesis is similar in L and HeLa cells and is markedly concentration-dependent in the low dose range (5-20 muM or 1.6-6.4 mug/ml), but not as higher concentrations of DRB. At a concentration of 12 muM, DRB has a highly selective inhibitory effect on the synthesis of nuclear heterogenous RNA in L cells. At higher concentrations, there is also inhibition of 45 S ribosomal precursor RNA synthesis, but at all concentrations the effect on heterogeneous RNA synthesis in L cells in considerably greater than that on preribosomal RNA synthesis. In HeLa cells, too, DRB has a selective effect on heterogeneous RNA synthesis, but quantitatively the selectivity of action is somewhat less pronounced. In both L and HeLa cells, the inhibition of synthesis of nuclear heterogeneous RNA is incomplete even at very high concentrations of DRB (150 muM). Thus, while DRB is a selective inhibitor of nuclear heterogeneous RNA synthesis, not all such RNA synthesis is sensitive to inhibition. It is proposed that messenger precursor RNA synthesis may largely be sensitive to inhibition by DRB. In short-term experiments, DRB has no effect on protein synthesis in L or HeLa cells. DRB has a slight to moderate inhibitory effect on uridine uptake into L cells and a moderate to marked effect on uptake of uridine into HeLa cells.

Relative Resistance to the Hypertensive Effects of Desoxycorticosterone During Active Phase of Renal Compensatory Hypertrophy

1958 ◽  
Vol 194 (2) ◽  
pp. 236-240 ◽  
Author(s):  
C. E. Hall ◽  
O. Hall
Keyword(s):  
Active Phase ◽  
Hormone Treatment ◽  
Compensatory Hypertrophy ◽  
Renal Tubules ◽  
Sodium Retention ◽  
Relative Resistance ◽  
Renal Hypertrophy ◽  
Kidney Size ◽  
Compensatory Renal Hypertrophy ◽  
Desoxycorticosterone Acetate

An attempt was made to ascertain the circumstances under which unilateral nephrectomy maximally sensitized rats to hypertensive cardiovascular disease induced by desoxycorticosterone acetate in the presence of augmented NACl intake. The experiments showed that animals in which hormone treatment was delayed until 2 weeks after uninephrectomy were much more sensitive than animals in which hormone treatment was begun on the day of kidney removal. This was indicated by earlier onset and greater severity of hypertension; by a larger percentage of animals in such groups being affected, and by a greater incidence and severity of cardiovascular lesions in the former as compared with the latter. The much greater kidney size of the former clearly makes it difficult to ascribe the greater sensitivity to a reduction in renal mass as such. It is thought that during active compensatory renal hypertrophy the renal tubules are probably less responsive to the action of the hormone and therefore less prone to develop sodium retention and hence hypertension.

Endothelial dysfunction promotes the transition from compensatory renal hypertrophy to kidney injury after unilateral nephrectomy in mice

2012 ◽  
Vol 302 (11) ◽  
pp. F1402-F1408 ◽  
Author(s):  
Hajime Nagasu ◽  
Minoru Satoh ◽  
Kengo Kidokoro ◽  
Yuko Nishi ◽  
Keith M. Channon ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Soluble Guanylate Cyclase ◽  
Kidney Injury ◽  
Compensatory Hypertrophy ◽  
Initiation Factor ◽  
Unilateral Nephrectomy ◽  
Wild Type ◽  
Renal Hypertrophy ◽  
No Donor ◽  
Compensatory Renal Hypertrophy

Loss of functional nephrons associated with chronic kidney disease induces glomerular hyperfiltration and compensatory renal hypertrophy. We hypothesized that the endothelial nitric oxide synthase (eNOS) [soluble guanylate cyclase (sGC)] protein kinase G (PKG) pathway plays an important role in compensatory renal hypertrophy after unilateral nephrectomy. Analysis of mice subjected to unilateral nephrectomy showed increases in kidney weight-to-body weight and total protein-to-DNA ratios in wild-type but not eNOS knockout (eNOSKO) mice. Serum creatinine and blood urea nitrogen increased after nephrectomy in eNOSKO but not in wild-type mice. Furthermore, Bay 41–2272, an sGC stimulator, induced compensatory renal hypertrophy in eNOSKO mice and rescued renal function. The NO donor S-nitrosoglutathione (GSNO) and Bay 41–2272 stimulated PKG activity and induced phosphorylation of Akt protein in human proximal tubular cells. GSNO also induced phosphorylation of eukaryotic initiation factor 4E-binding protein and ribosomal protein S6. Our results highlight the importance of the eNOS-NO-PKG pathway in compensatory renal hypertrophy and suggest that reduced eNOS-NO bioavailability due to endothelial dysfunction is the underlying mechanism of failure of compensatory hypertrophy and acceleration of progressive renal dysfunction.

scholarly journals THE DEGREE OF COMPENSATORY RENAL HYPERTROPHY FOLLOWING UNILATERAL NEPHRECTOMY

1932 ◽  
Vol 56 (2) ◽  
pp. 255-265 ◽  
Author(s):  
E. M. MacKay ◽  
L. L. MacKay ◽  
T. Addis
Keyword(s):  
Adult Life ◽  
Compensatory Hypertrophy ◽  
Rapid Decrease ◽  
Unilateral Nephrectomy ◽  
Albino Rats ◽  
Renal Hypertrophy ◽  
Compensatory Renal Hypertrophy

Compensatory hypertrophy of the kidney in albino rats becomes less as age advances. There is a rapid decrease from 5 days to 60 days of age and then a slow diminution throughout adult life.

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