Retardation of thyroxine-induced metamorphosis by amphenone B in toad tadpoles.

Kikuyama, Sakaé; Niki, Kaoru; Mayumi, Masako; Kawamura, Kazushi

doi:10.1507/endocrj1954.29.659

Cited by 24 publications

(8 citation statements)

References 10 publications

(5 reference statements)

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“…A number of thyroid hormone-driven events during climax of metamorphosis are accelerated by glucocorticoids (see reviews in Kikuyama et al, 1993;and Kaltenbach, 1996 it may not be surprising that inhibition of glucocorticoid receptor binding by RU486 has the general effect of delaying metamorphic progression. Our results are consistent with the previous observation of Kikuyama and co-workers that treatment of metamorphosing tadpoles with an agent that inhibits corticosteroid synthesis (Amphenone B) delays resorption of the tail (Kikuyama et al, 1982). The increase in wet weight following RU486 treatment is thought to be due to increased water retention.…”

Section: Discussionsupporting

confidence: 93%

Involvement of Glucocorticoids in the Reorganization ofthe Amphibian Immune System at Metamorphosis

Rollins‐Smith

Barker

Davis

1997

Journal of Immunology Research

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In recent years, integrative animal biologists and behavioral scientists have begun to understand the complex interactions between the immune system and the neuroendocrine system. Amphibian metamorphosis offers a unique opportunity to study dramatic hormone-driven changes in the immune system in a compressed time frame. In the South African clawed frog, Xenopus laevis, the larval pattern of immunity is distinct from that of the adult, and metamorphosis marks the transition from one pattern to the other. Climax of metamorphosis is characterized by significant elevations in thyroid hormones, glucocorticoid hormones, and the pituitary hormones, prolactin and growth hormone. Previously, we and others have shown that elevated levels of unbound glucocorticoid hormones found at climax of metamorphosis are associated with a natural decline in lymphocyte numbers, lymphocyte viability, and mitogen-induced proliferation. Here we present evidence that the mechanism for loss of lymphocytes at metamorphosis is glucocorticoid-induced apoptosis. Inhibition of lymphocyte function and loss of lymphocytes in the thymus and spleen are reversible by in vitro or in vivo treatment with the glucocorticoid receptor antagonist, RU486, whereas the mineralocorticoid receptor antagonist, RU26752, is poorly effective. These observations support the hypothesis that loss of larval lymphocytes and changes in lymphocyte function are due to elevated concentrations of glucocorticoids that remove unnecessary lymphocytes to allow for development of immunological tolerance to the new adult-specific antigens that appear as a result of metamorphosis.

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Section: Discussionsupporting

confidence: 93%

Involvement of Glucocorticoids in the Reorganization ofthe Amphibian Immune System at Metamorphosis

Rollins‐Smith

Barker

Davis

1997

Journal of Immunology Research

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“…Similar findings were obtained by others with tadpoles of different anuran species including X. laevis (Gray and Janssens, 1990; reviewed by Denver, 2009a; Kikuyama et al, 1993). A physiological role for CS in tadpole metamorphosis is supported by the findings of Kikuyama et al (1982) who showed that treatment of tadpoles with the CS synthesis inhibitor amphenone B retarded T 4 -induced tail resorption, and that this could be reversed by treatment with CS. Several investigators reported synergistic actions between CS and TH in tadpole tail explants (Kikuyama et al, 1993; Kikuyama et al, 1983).…”

Section: Discussionmentioning

confidence: 81%

Molecular mechanisms of corticosteroid synergy with thyroid hormone during tadpole metamorphosis

Bonett

Hoopfer

Denver

2010

General and Comparative Endocrinology

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Corticosteroids (CS) act synergistically with thyroid hormone (TH) to accelerate amphibian metamorphosis. Earlier studies showed that CS increase nuclear 3,5,3′-triiodothyronine (T3) binding capacity in tadpole tail, and 5′ deiodinase activity in tadpole tissues, increasing the generation of T3 from thyroxine (T4). In the present study we investigated CS synergy with TH by analyzing expression of key genes involved in TH and CS signaling using tadpole tail explant cultures, prometamorphic tadpoles, and frog tissue culture cells (XTC-2 and XLT-15). Treatment of tail explants with T3 at 100 nM, but not at 10 nM caused tail regression. Corticosterone (CORT) at three doses (100, 500, 3400 nM) had no effect or increased tail size. T3 at 10 nM plus CORT caused tails to regress similar to 100 nM T3. Thyroid hormone receptor beta (TRβ) mRNA was synergistically upregulated by T3 plus CORT in tail explants, tail and brain in vivo, and tissue culture cells. The activating 5′ deiodinase type 2 (D2) mRNA was induced by T3 and CORT in tail explants and tail in vivo. Thyroid hormone increased expression of glucocorticoid (GR) and mineralocorticoid receptor (MR) mRNAs. Our findings support that the synergistic actions of TH and CS in metamorphosis occur at the level of expression of genes for TRβ and D2, enhancing tissue sensitivity to TH. Concurrently, TH enhances tissue sensitivity to CS by upregulating GR and MR. Environmental stressors can modulate the timing of tadpole metamorphosis in part by CS enhancing the response of tadpole tissues to the actions of TH.

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“…However, treatment with a graded series of TH from low to high over successive days to mimic the developmental profile of endogenous plasma TH enables complete metamorphosis including tail resorption, and TH alone induces nearly complete tail shrinkage in culture devoid of other hormones (37, 53, 82). Even though GCs have no known action to induce tail regression, GCs synergize with TH in vitro to accelerate tail shrinkage (14, 83) and inhibition of GC signaling with amphenone B (a corticoid synthesis inhibitor) inhibited TH-induced tail resorption in vivo (84). In contrast, cortisol partly inhibited TH-induced reduction in DNA synthesis in tail epidermal cells (85), which is consistent with the observation that GCs by themselves increase tail growth in vitro (14, 83).…”

Section: Analysis Of the Sufficiency Of Th/tr Signaling In Frog Metammentioning

confidence: 99%

Insufficiency of Thyroid Hormone in Frog Metamorphosis and the Role of Glucocorticoids

Sachs

Buchholz

2019

Front. Endocrinol.

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Thyroid hormone (TH) is the most important hormone in frog metamorphosis, a developmental process which will not occur in the absence of TH but can be induced precociously by exogenous TH. However, such treatments including in-vitro TH treatments often do not replicate the events of natural metamorphosis in many organs, including lung, brain, blood, intestine, pancreas, tail, and skin. A potential explanation for the discrepancy between natural and TH-induced metamorphosis is the involvement of glucocorticoids (GCs). GCs are not able to advance development by themselves but can modulate the rate of developmental progress induced by TH via increased tissue sensitivity to TH. Global gene expression analyses and endocrine experiments suggest that GCs may also have direct actions required for completion of metamorphosis independent of their effects on TH signaling. Here, we provide a new review and analysis of the requirement and necessity of TH signaling in light of recent insights from gene knockout frogs. We also examine the independent and interactive roles GCs play in regulating morphological and molecular metamorphic events dependent upon TH.

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Retardation of thyroxine-induced metamorphosis by amphenone B in toad tadpoles.

Cited by 24 publications

References 10 publications

Involvement of Glucocorticoids in the Reorganization ofthe Amphibian Immune System at Metamorphosis

Involvement of Glucocorticoids in the Reorganization ofthe Amphibian Immune System at Metamorphosis

Molecular mechanisms of corticosteroid synergy with thyroid hormone during tadpole metamorphosis

Insufficiency of Thyroid Hormone in Frog Metamorphosis and the Role of Glucocorticoids

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