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Title: Age-related failure of endocytosis may be the pathogenetic mechanism responsible for cold follicle formation in the aging mouse thyroid

Abstract

With advancing age, 60-80% of the follicles of the mouse thyroid gland turn cold, i.e. they lose their normal capacity to iodinate thyroglobulin (Tgb). Cold follicles are morphologically characterized by their large size, by deeply periodic acid-Schiff-stained colloid and by flat epithelial cells. We investigated the hypothesis that a progressive, age-related failure of endocytosis, leading to a gradually increasing mismatch between production of new Tgb and resorption of stored Tgb, could lead to overfilling of colloid stores with consecutive impediment of diffusion. To this purpose, labeling of the thyroids was started when mice were 3 months old, and 125I was continuously administered thereafter for 2-6 months. After this time, all follicles were homogeneously labeled in autoradiographs. Tracer application was then discontinued. Autoradiographs obtained at intervals during the washout of the tracer yielded a mirror image of that observed after acute labeling. The large follicles which were cold after acute labeling in old animals now still retained labeled iodoproteins even after 7 weeks of washout, i.e. at a time when morphologically normal follicles had long lost their labeled Tgb stores. Thus, the cold follicles of the old thyroid must have been functioning normally during equilibration of young thyroids, but have thenmore » gradually lost their capacity to iodinate and to remove stored Tgb from the colloid. The observation supports the thesis that aging primarily affects the cytoskeleton and, thus, the cell's endocytotic machinery. This effect of aging on the thyroid can be prevented by life-long stimulation of the gland by TSH.« less

Authors:
; ;
Publication Date:
Research Org.:
Univ. Clinic of Internal Medicine, Inselspital, Bern, Switzerland
OSTI Identifier:
6468135
Resource Type:
Journal Article
Journal Name:
Endocrinology; (United States)
Additional Journal Information:
Journal Volume: 5
Country of Publication:
United States
Language:
English
Subject:
59 BASIC BIOLOGICAL SCIENCES; AGING; BIOLOGICAL EFFECTS; THYROGLOBULIN; TISSUE DISTRIBUTION; THYROID; LABELLING; MORPHOLOGICAL CHANGES; AUTORADIOGRAPHY; CHLORATES; IODINE; MICE; PATHOGENESIS; RATS; THYROXINE; TRIIODOTHYRONINE; TSH; AMINO ACIDS; ANIMALS; BODY; CARBOXYLIC ACIDS; CHLORINE COMPOUNDS; DISTRIBUTION; ELEMENTS; ENDOCRINE GLANDS; GLANDS; GLOBULINS; HALOGEN COMPOUNDS; HALOGENS; HORMONES; MAMMALS; NONMETALS; ORGANIC ACIDS; ORGANIC COMPOUNDS; ORGANIC HALOGEN COMPOUNDS; ORGANIC IODINE COMPOUNDS; ORGANS; OXYGEN COMPOUNDS; PEPTIDE HORMONES; PITUITARY HORMONES; PROTEINS; RODENTS; THYROID HORMONES; VERTEBRATES; 551001* - Physiological Systems- Tracer Techniques

Citation Formats

Gerber, H., Peter, H.J., and Studer, H. Age-related failure of endocytosis may be the pathogenetic mechanism responsible for cold follicle formation in the aging mouse thyroid. United States: N. p., 1987. Web. doi:10.1210/endo-120-5-1758.
Gerber, H., Peter, H.J., & Studer, H. Age-related failure of endocytosis may be the pathogenetic mechanism responsible for cold follicle formation in the aging mouse thyroid. United States. doi:10.1210/endo-120-5-1758.
Gerber, H., Peter, H.J., and Studer, H. Fri . "Age-related failure of endocytosis may be the pathogenetic mechanism responsible for cold follicle formation in the aging mouse thyroid". United States. doi:10.1210/endo-120-5-1758.
@article{osti_6468135,
title = {Age-related failure of endocytosis may be the pathogenetic mechanism responsible for cold follicle formation in the aging mouse thyroid},
author = {Gerber, H. and Peter, H.J. and Studer, H.},
abstractNote = {With advancing age, 60-80% of the follicles of the mouse thyroid gland turn cold, i.e. they lose their normal capacity to iodinate thyroglobulin (Tgb). Cold follicles are morphologically characterized by their large size, by deeply periodic acid-Schiff-stained colloid and by flat epithelial cells. We investigated the hypothesis that a progressive, age-related failure of endocytosis, leading to a gradually increasing mismatch between production of new Tgb and resorption of stored Tgb, could lead to overfilling of colloid stores with consecutive impediment of diffusion. To this purpose, labeling of the thyroids was started when mice were 3 months old, and 125I was continuously administered thereafter for 2-6 months. After this time, all follicles were homogeneously labeled in autoradiographs. Tracer application was then discontinued. Autoradiographs obtained at intervals during the washout of the tracer yielded a mirror image of that observed after acute labeling. The large follicles which were cold after acute labeling in old animals now still retained labeled iodoproteins even after 7 weeks of washout, i.e. at a time when morphologically normal follicles had long lost their labeled Tgb stores. Thus, the cold follicles of the old thyroid must have been functioning normally during equilibration of young thyroids, but have then gradually lost their capacity to iodinate and to remove stored Tgb from the colloid. The observation supports the thesis that aging primarily affects the cytoskeleton and, thus, the cell's endocytotic machinery. This effect of aging on the thyroid can be prevented by life-long stimulation of the gland by TSH.},
doi = {10.1210/endo-120-5-1758},
journal = {Endocrinology; (United States)},
number = ,
volume = 5,
place = {United States},
year = {1987},
month = {5}
}