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Thyroid hormone differentially regulates cellular development in neonatal rat heart and kidney
T A Slotkin1, F J Seidler, R J Kavlock
1Department of Pharmacology, Duke University Medical Center, Durham, North Carolina 27710.
Insights
Thyroid hormone significantly impacts cardiac and renal cell development. Triiodothyronine (T3) selectively promotes heart cell proliferation, while propylthiouracil (PTU) impairs cell growth in both organs.
Area of Science:
- Endocrinology
- Developmental Biology
- Cardiovascular Physiology
- Renal Physiology
Background:
- Thyroid hormone is crucial for normal development and organ function.
- Its specific roles in cardiac and renal cell development require further elucidation.
Purpose of the Study:
- To investigate the effects of hyperthyroidism and hypothyroidism on cardiac and renal cell development in neonatal rats.
- To differentiate the impacts of thyroid hormone on cell number, packing density, and size.
Main Methods:
- Neonatal rats were made hyperthyroid using triiodothyronine (T3) or hypothyroid using propylthiouracil (PTU).
- Cell number (DNA), cell packing density (DNA/g), and cell size (protein/DNA) were measured in cardiac and renal tissues.
- Measurements were taken from birth through young adulthood.
Main Results:
- Propylthiouracil (PTU) induced comparable deficits in cell number in both heart and kidney, with longer persistence in the kidney.
- Triiodothyronine (T3) selectively caused cardiac overgrowth, increasing cell number and size, while impairing general growth.
- Hypothyroid-induced deficits in cell packing and size were secondary to reduced cell number.
Conclusions:
- Thyroid hormone differentially regulates cardiac and renal cell development.
- T3 promotes cardiac hyperplasia in developing animals, a unique effect not seen in adults.
- Hypothyroidism broadly impacts cell number in both organs, with distinct recovery dynamics.
Abstract:
The role of thyroid hormone in the control of cardiac and renal cell development was examined in neonatal rats made hyperthyroid by administration of triiodothyronine (T3, 0.1 mg/kg s.c. on postnatal days 1-5) or hypothyroid by administration of propylthiouracil (PTU, 20 mg/kg s.c. given to dams on gestational day 17 through postnatal day 5 and to pups on postnatal days 1-5). Indices of total cell number (total DNA per tissue), cell packing density (DNA per g tissue), and relative cell size (protein/DNA ratio) were evaluated from birth through young adulthood. PTU administration led to primary shortfalls in cell number that were of similar magnitude in both tissues, but persisted somewhat longer in the kidney than in the heart. Deficits in cell packing density and cell size in the hypothyroid animals were secondary to the effect on cell number, displaying smaller magnitudes of effect and a lag in appearance and disappearance of the deficits compared to that for total DNA; indeed, the phase in which tissues were restoring their cell numbers was accompanied by increased cell packing density, reflecting a more rapid restitution of cell numbers than tissue weight or cell size. In contrast to the relatively similar effects of PTU on developing cardiac and renal cells, the effects of T3 were selective for the heart. Although T3 caused general growth impairment, it evoked marked cardiac overgrowth that was accompanied by a striking increase in cell number and a small increase in cell size. The cardiac hyperplasia is unique to the developing animal, as post-replicative heart cells in adult animals show only hypertrophy in response to thyroid hormone.(ABSTRACT TRUNCATED AT 250 WORDS)