Polyamines and nucleic acids in the mouse kidney induced to growth by testosterone propionate

Henningsson, Stig; Persson, Lo; Rosengren, E.

doi:10.1111/j.1748-1716.1978.tb06085.x

Cited by 52 publications

(19 citation statements)

References 22 publications

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“…This contrasts with results in castrated mice [4] and is pos sibly explained by the inhibitory effect of endogenous steroids noted by Kochakian [9]. However, the increased kidney weights of the chronically treated mice indicate that the anabolic properties of testosterone were ac tive (table I).…”

Section: Methodscontrasting

confidence: 50%

Effects of Testosterone on Renal Ornithine Decarboxylase and Kidney Function

Ka¹,

Je²,

Jj³

1982

Enzyme

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Testosterone injection caused a 2,000% increase in renal ornithine decarboxylase activity in intact male mice. A single injection of testosterone produced the same effect as repeated injections. The response was dose-dependent and could be blocked by actinomycin, diaminopropane, and cadaverine. Cycloheximide and putrescine had no inhibitory effect. Renal ODC response to arginine vasopressin was altered after castration; however, urine specific gravity and serum osmolality were unaffected by changes in renal ornithine decarboxylase activity.

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Section: Methodscontrasting

confidence: 50%

Effects of Testosterone on Renal Ornithine Decarboxylase and Kidney Function

Ka¹,

Je²,

Jj³

1982

Enzyme

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“…Testosterone administration markedly increases the activity of OrnDCase and other proteins in mouse kidney (5,6,14,15,(33)(34)(35) and produces cellular hypertrophy rather than hyperplasia (35). The induction requires functional androgen receptors and is seen as early as a few hours after hormone administration (5,34).…”

Section: Discussionmentioning

confidence: 99%

Androgen induction of ornithine decarboxylase mRNA in mouse kidney as studied by complementary DNA.

Kontula¹,

Torkkeli²,

Bardin³

et al. 1984

Proc. Natl. Acad. Sci. U.S.A.

162

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To investigate the mechanisms by which androgens regulate ornithine decarboxylase (OrnDCase; L-ornithine carboxy-lyase, EC 4.1.1.17) in mouse kidney, a cDNA clone encoding OrnDCase mRNA was prepared. Purification of OrnDCase mRNA from kidneys of androgen-treated mice was accomplished by immunoadsorption of renal polysomes to a protein A-Sepharose column and enrichment for poly(A)-containing RNA by oligo(dT)-cellulose. Double-stranded cDNA synthesized from this mRNA was inserted into the Pst I site of plasmid pBR322 by using oligo(dGdC)-tailing and was propagated in Escherichia coli. Plasmids containing cDNA sequences coding for OrnDCase were identified by differential colony hybridization, by radioimmunological detection of OrnDCase-like antigens in bacterial cultures, and by cell-free translation of hybrid-selected mRNA followed by imununoprecipitation with monospecific OrnDCase antiserun%. A restriction endonuclease fragment of the selected plasmid DNA (pODCS4) was labeled by nick-translation and used to study changes in OrnDCase mRNA concentration. After a single dose of testosterone, renal OrnDCase mRNA concentration increased as soon as 6 hr and peaked 24 hr after steroid injection, as measured by RNA blot hybridization. Continuous androgen treatment for 4 days resulted in a 10-to 20-fold increase in OrnDCase mRNA concentration in normal animals, but no induction of this mRNA was detected in mice that have an inherent defect of the androgen receptor (testicular feminization). These results indicate that androgens regulate OrnDCase synthesis in mouse kidney, at least in part, by increasing OrnDCase mRNA accumulation.Ornithine decarboxylase (OrnDCase; L-ornithine carboxylyase, EC 4.1.1.17) catalyzes the conversion of ornithine to putrescine and is the first and apparently rate-limiting enzyme in polyamine biosynthesis. A striking feature of this enzyme is that it has extremely rapid induction kinetics and a high turnover rate (for review, see refs. 1-4). Several studies (1-6) have suggested that regulation of OrnDCase activity occurs through modulation of the amount of the enzyme protein, although other factors such as inhibitors (7-10) or activators (11) of OrnDCase and post-translational enzyme modifications (12, 13) also may be involved. A major reason for difficulties in studying the regulation of this enzyme is that it represents only 0.01-0.05% of the total cellular protein, even when maximally induced. Nonetheless, purification of the enzyme to apparent homogeneity (5,(14)(15)(16)(17) and development of radioimmunoassays (5, 6) have permitted studies on OrnDCase turnover.We reasoned that further understanding of the factors that regulate OrnDCase would be facilitated if a probe were available that would allow direct measurement of OrnDCase mRNA sequences. Kidneys of testosterone-treated mice were chosen as a source for isolation of OrnDCase mRNA because androgen administration increases enzyme protein in this organ to a higher concentration than is known in most tissues (2, 5, 6). In the presen...

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“…In this regard, it is known that there is a marked sexual extra-genital dimorphism in the kidney, liver, and skeletal muscle in several mouse strains, affecting many different proteins (Bardin & Catterall 1981). In particular, renal ornithine decarboxylase (ODC) activity is remarkably higher in males than in females, and the treatment of females with testosterone elicits a dramatic increase of ODC activity in renal tissue (Henningsson et al 1978, Melatinou et al 1987, Sánchez-Capelo et al 1994, mediated by transcriptional, translational, and post-translational mechanisms (Seely et al 1982, Kontula et al 1984, Berger & Watson 1989. On the other hand, renal histidine decarboxylase is up-regulated by estrogens and repressed by androgens (Grahn et al 1973, Middleton et al 1987, Middleton & Bulfield 1988.…”

Section: Introductionmentioning

confidence: 99%

Opposite sexual dimorphism of 3,4-dihydroxyphenylalanine decarboxylase in the kidney and small intestine of mice

López-Contreras

Galindo²,

López‐García³

et al. 2007

Journal of Endocrinology

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3,4-Dihydroxyphenylalanine decarboxylase (DDC; also known as L-amino acid decarboxylase) is involved in the synthesis of dopamine, norepinephrine, and serotonin, and also acts as an androgen receptor co-regulator protein. In contrast to other amino acid decarboxylases that are modulated by sex hormones, little is known about the influence of these hormones on DDC regulation. In the present work, we studied the influence of gender in the expression of DDC in different mouse tissues. Among the different organs studied, including brain, liver, kidney, intestine, heart, adrenal gland, and skeletal muscle, only kidney and small intestine showed a sex-dependent dimorphism in DDC expression. In the kidney, levels of DDC activity, DDC mRNA, and protein were remarkably higher in females than in males. On the contrary, in the small intestine, male mice displayed higher levels of DDC activity than females but they did not correlate precisely with mRNA levels. This dimorphism was dependent on androgens, since male castration and treatment of female mice with testosterone propionate, oppositely affected DDC levels in kidney and small intestine. However, estrogen ablation or treatment with estradiol did not significantly affect DDC activity in these tissues. Immunocytochemical analysis revealed that DDC was mainly located in the proximal straight tubular cells of the kidney and in the cytoplasm of enterocytes. These data and the fact that renal DDC inversely correlated with renal sodium reabsorption suggest that renal and intestinal gender dimorphism in DDC could be related to sexrelated differences in sodium balance observed between males and females.

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Polyamines and nucleic acids in the mouse kidney induced to growth by testosterone propionate

Cited by 52 publications

References 22 publications

Effects of Testosterone on Renal Ornithine Decarboxylase and Kidney Function

Effects of Testosterone on Renal Ornithine Decarboxylase and Kidney Function

Androgen induction of ornithine decarboxylase mRNA in mouse kidney as studied by complementary DNA.

Opposite sexual dimorphism of 3,4-dihydroxyphenylalanine decarboxylase in the kidney and small intestine of mice

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