The mitochondrion as a primary site of action of steroid and thyroid hormones: Presence and action of steroid and thyroid hormone receptors in mitochondria of animal cells

2006 ◽  
Vol 246 (1-2) ◽  
pp. 21-33 ◽  
Author(s):  
A.-M.G. Psarra ◽  
S. Solakidi ◽  
C.E. Sekeris
2020 ◽  
Vol 244 (1) ◽  
pp. 83-94 ◽  
Author(s):  
Ángela Sánchez ◽  
Constanza Contreras-Jurado ◽  
Diego Rodríguez ◽  
Javier Regadera ◽  
Susana Alemany ◽  
...  

Hypothyroidism is often associated with anemia and immunological disorders. Similar defects are found in patients and in mice with a mutated dominant-negative thyroid hormone receptor α (TRα) and in knockout mice devoid of this receptor, suggesting that this isoform is responsible for the effects of the thyroid hormones in hematopoiesis. However, the hematological phenotype of mice lacking also TRβ has not yet been examined. We show here that TRα1/TRβ-knockout female mice, lacking all known thyroid hormone receptors with capacity to bind thyroid hormones, do not have overt anemia and in contrast with hypothyroid mice do not present reduced Gata1 or Hif1 gene expression. Similar to that found in hypothyroidism or TRα deficiency during the juvenile period, the B-cell population is reduced in the spleen and bone marrow of ageing TRα1/TRβ-knockout mice, suggesting that TRβ does not play a major role in B-cell development. However, splenic hypotrophy is more marked in hypothyroid mice than in TRα1/TRβ-knockout mice and the splenic population of T-lymphocytes is not significantly impaired in these mice in contrast with the reduction found in hypothyroidism. Our results show that the overall hematopoietic phenotype of the TRα1/TRβ-knockout mice is milder than that found in the absence of hormone. Although other mechanism/s cannot be ruled out, our results suggest that the unoccupied TRs could have a negative effect on hematopoiesis, likely secondary to repression of hematopoietic gene expression.


1997 ◽  
Vol 9 (5) ◽  
pp. 489 ◽  
Author(s):  
Conrad Sernia ◽  
Tang Zeng ◽  
Robert T. Gemmell

Newborn marsupials do not have a thyroid gland at birth. The gland develops while the young marsupial is in the mother’s pouch. The young brushtail possum initiates secretion of thyroid hormones from its own thyroid at about Day 65 post partum. However, during the first three weeks of pouch life thyroxine is passed from the mother to the young via the milk. To determine if this maternal thyroxine can effect organ development in the young possum before it initiates secretion of thyroxine from its own thyroid, the ontogeny of thyroid hormone receptors was determined in nuclear extracts of lung, liver and kidney by radioreceptor assay, using125I-labelled tri-iodothyronine as ligand. Receptor density was calculated for tissues removed from young possums at Days 25 (n = 5), 50 (n = 4), 100 (n = 3) and 150 (n = 4) and from adults (n = 5). Receptors were found in possums of all age groups, including the small 25-day pouch young. Significant differences were not found in the receptor density between different tissues or at various ages. The association constant Ka (4 ·0 ± 2· 6 L nmol-1 for lung) was similar in different tissues and at the various ages examined. The passage of thyroid hormones from the mother to the developing marsupial via the milk may have a role in the slow development of organ systems early in pouch life by acting on thyroid receptors in the pouch young. However, the functional maturation of the thyroid gland of the young possum, not an increase in receptors, appears to coincide with the rapid increase in the rate of growth and development which occurs in later pouch life.


2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Łukasz Szymański ◽  
Damian Matak ◽  
Ewa Bartnik ◽  
Cezary Szczylik ◽  
Anna M. Czarnecka

It is known that thyroid hormone is an important regulator of cancer development and metastasis. What is more, changes across the genome, as well as alternative splicing, may affect the activity of the thyroid hormone receptors. Mechanism of action of the thyroid hormone is different in every cancer; therefore in this review thyroid hormone and its receptor are presented as a regulator of renal cell carcinoma.


2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Gabriel Fernandes Silveira ◽  
Andréia Buffon ◽  
Alessandra Nejar Bruno

It is known that thyroid hormones influence a wide variety of events at the molecular, cellular, and functional levels. Thyroid hormones (TH) play pivotal roles in growth, cell proliferation, differentiation, apoptosis, development, and metabolic homeostasis via thyroid hormone receptors (TRs) by controlling the expression of TR target genes. Most of these effects result in pathological and physiological events and are already well described in the literature. Even so, many recent studies have been devoted to bringing new information on problems in controlling the synthesis and release of these hormones and to elucidating mechanisms of the action of these hormones unconventionally. The purinergic system was recently linked to thyroid diseases, including enzymes, receptors, and enzyme products related to neurotransmitter release, nociception, behavior, and other vascular systems. Thus, throughout this text we intend to relate the relationship between the TH in physiological and pathological situations with the purinergic signaling.


1993 ◽  
Vol 59 (6) ◽  
pp. 1187-1190 ◽  
Author(s):  
Anthony N. Wakim ◽  
Sandra L. Polizotto ◽  
Mary Jo Buffo ◽  
Miguel A. Marrero ◽  
Dennis R. Burholt

Molecules ◽  
2021 ◽  
Vol 26 (23) ◽  
pp. 7337
Author(s):  
Lorena Tedeschi ◽  
Cristina Vassalle ◽  
Giorgio Iervasi ◽  
Laura Sabatino

The thyroid hormone receptors are the mediators of a multitude of actions by the thyroid hormones in cells. Most thyroid hormone activities require interaction with nuclear receptors to bind DNA and regulate the expression of target genes. In addition to genomic regulation, thyroid hormones function via activation of specific cytosolic pathways, bypassing interaction with nuclear DNA. In the present work, we reviewed the most recent literature on the characteristics and roles of different factors involved in thyroid hormone function in particular, we discuss the genomic activity of thyroid hormone receptors in the nucleus and the functions of different thyroid hormone receptor isoforms in the cytosol. Furthermore, we describe the integrin αvβ3-mediated thyroid hormone signaling pathway and its rapid nongenomic action in the cell. We furthermore reviewed the thyroid hormone transporters enabling the uptake of thyroid hormones in the cell, and we also include a paragraph on the proteins that mediate thyroid receptors’ shuttling from the nucleus to the cytosol.


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