Triiodothyronine (T3) does not induce Rankl expression in rat Ros 17/2.8 cells

Saraiva, Patrícia Pinto; Teixeira, S. S.; Nogueira, Célia Regina; Padovani, Carlos Roberto

doi:10.1590/s0004-27302008000100015

Cited by 10 publications

(3 citation statements)

References 15 publications

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“…Similarly, treatment of immortalized osteoblasts or primary bone marrow stromal cells resulted in increased RANKL, interleukin 6 (IL-6), IL-8 and prostaglandin E2 expression, and inhibition of OPG, consistent with an indirect effect of thyroid hormones on osteoclast function (254,258,266). Other studies, however, suggest effects of T3 on osteoclastogenesis are independent of RANKL signaling (273,274). A further complication is that while TR expression is well documented in osteoblastic cells, some of the effects of T3 on bone organ cultures are extremely rapid and involve mobilization of intracellular calcium stores to suggest that nongenomic TR-independent actions of T3 may be relevant (275).…”

Section: Osteoclastsmentioning

confidence: 75%

Role of Thyroid Hormones in Skeletal Development and Bone Maintenance

2016

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The skeleton is an exquisitely sensitive and archetypal T3-target tissue that demonstrates the critical role for thyroid hormones during development, linear growth, and adult bone turnover and maintenance. Thyrotoxicosis is an established cause of secondary osteoporosis, and abnormal thyroid hormone signaling has recently been identified as a novel risk factor for osteoarthritis. Skeletal phenotypes in genetically modified mice have faithfully reproduced genetic disorders in humans, revealing the complex physiological relationship between centrally regulated thyroid status and the peripheral actions of thyroid hormones. Studies in mutant mice also established the paradigm that T3 exerts anabolic actions during growth and catabolic effects on adult bone. Thus, the skeleton represents an ideal physiological system in which to characterize thyroid hormone transport, metabolism, and action during development and adulthood and in response to injury. Future analysis of T3 action in individual skeletal cell lineages will provide new insights into cell-specific molecular mechanisms and may ultimately identify novel therapeutic targets for chronic degenerative diseases such as osteoporosis and osteoarthritis. This review provides a comprehensive analysis of the current state of the art.

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Section: Osteoclastsmentioning

confidence: 75%

Role of Thyroid Hormones in Skeletal Development and Bone Maintenance

2016

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“…OPG is a decoy receptor that inhibits receptor activator of nuclear factor-B ligand (RANKL) mediated activation of osteoclastogenesis [63] . However, the involvement of T3 in regulation of the OPG/ RANKL pathway is controversial as other studies suggest effects of T3 on osteoclastogenesis may be independent of RANKL [64,65] . Thus, although thyrotoxicosis results in increased osteoclast numbers and activity leading to increased bone resorption in vivo, it is not clear whether T3 acts directly in osteoclasts or whether these responses are secondary to direct actions of T3 in osteoblasts.…”

Section: Thyroid Hormone Action In Osteoblastsmentioning

confidence: 99%

Thyroid Hormone Actions in Cartilage and Bone

Williams¹

2012

Eur Thyroid J

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T3 action in bone are considered in relation to mutant mouse models and to effects on bone mineral density and fracture susceptibility in humans. Finally, new studies identifying a putative role for thyroid hormone metabolism in articular cartilage maintenance and the pathogenesis of osteoarthritis are considered. The pharmacological context of these new findings is discussed, emphasising the importance of this emerging field of study in thyroid hormone pathophysiology.Copyright © 2012 European Thyroid Association Published by S. Karger AG, Basel Regulation of Thyroid Hormone Action Hypothalamic-Pituitary-Thyroid AxisThe thyroid gland produces mainly the pro-hormone T4 (3,5,3 ,5 -L -tetraiodothyronine, thyroxine) but also secretes smaller amounts of the active hormone T3 (3,5,3 -L -triiodothyronine). Most circulating T3 is derived via metabolism of T4, from which an outer-ring iodine atom is removed by activity of the type 1 iodothyronine deiodinase enzyme (Dio1) principally in liver and kidney [1] . The hypothalamic-pituitary-thyroid (HPT) axis senses circulating thyroid hormone concentrations and physiological thyroid status is controlled by negative feedback Key WordsThyroid hormone ؒ Cartilage ؒ Chondrocyte ؒ Ossification ؒ Osteoarthritis ؒ Bone ؒ Bone turnover ؒ Osteoblast ؒ Osteoclast ؒ Osteoporosis Abstract Thyroid hormones exert widespread and complex actions in almost all tissues during development, throughout childhood and in adults. The skeleton is an important T3-target tissue that exemplifies these processes, and yet understanding of the specific cellular and molecular mechanisms of T3 action in bone and cartilage remains incomplete. Here, the skeleton is considered as a T3-target tissue. The actions of thyroid hormones during skeletal development and in chondrocytes and growth plate cartilage during post-natal linear growth are outlined. The physiological importance of these actions are discussed in relation to patients with autosomal dominant mutations in genes encoding the thyroid hormone receptors TR ␣ 1 and TR ␤ , and in mice harbouring deletions or mutations of the orthologous genes. The role of thyroid hormones and the control of T3 action in bone turnover and maintenance are also outlined, and T3 action in boneforming osteoblasts and bone-resorbing osteoclasts discussed. The physiological and functional consequences of

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“…T 3 also stimulates the differentiation of osteoblasts, the synthesis and mineralization of the bone matrix; These effects are carried out through the regulation of procollagen enzymes, including bone alkaline phosphatase, and metalloproteinases 9 and 13 7 . It is not yet clear whether these effects are mediated via the activator receptor ligand pathway For nuclear factor B (RANKL) 8 , although studies with cell cultures of osteoblasts or precursors, demonstrate that T 3 increases the expression of RANKL and interleukins 6 and 8 9 .…”

Section: Ht Tsh and Bone Developmentmentioning

confidence: 99%

Hormonas tiroideas, TSH, cáncer de tiroides y hueso en mujeres pre y postmenopáusicas

Carranza

Iglesias

Díaz-Guerra

et al. 2017

Rev Osteoporos Metab Miner

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In recent years, progress has been made in regulating skeletal development and maintenance of bone mass of the adult by the hypothalamus-pituitary-thyroid axis. Studies have been carried out into the effect of thyroid hormones on the osteoblasts, osteoclast and the chondrocyte. This research has led to better genetic knowledge into the physiology of the cellular action of these hormones. Recently, possible D2 deodinase interventions in osteoporosis have been proposed. The link between bone mineral dignity, bone quality and the risk of fractures with thyroid hormones in normal postmenopausal women suggest a role for these hormones, even within the range of normal thyroid, in these diseases. On the other hand, the incidence of differentiated thyroid cancer, experimental in vivo thyroid hormone suppression by therapy, recurrent disease, has increased significantly. There are management guides, but it is clear that the secondary derivatives require a precise balance-adjusted indication, risk-benefit ratio of thyroid hormone dosage, prescribed long term, especially in cases of low tumor aggressiveness, advanced age and even in fragile patients. High risk patients should be referred for a bone densitometry, to consider treating future fractures. Prevention of osteoporosis, particularly in postmenopausal women, is highly desirable and should include adequate diet in calcium and vitamin D supplementation if necessary. There is still no consensus on osteoporosis treatment in the patient with thyroid cancer and suppressive treatment, but the indicated criteria for postmenopausal osteoporosis seem to be applicable in general.

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Triiodothyronine (T3) does not induce Rankl expression in rat Ros 17/2.8 cells

Cited by 10 publications

References 15 publications

Role of Thyroid Hormones in Skeletal Development and Bone Maintenance

Role of Thyroid Hormones in Skeletal Development and Bone Maintenance

Thyroid Hormone Actions in Cartilage and Bone

Hormonas tiroideas, TSH, cáncer de tiroides y hueso en mujeres pre y postmenopáusicas

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