Dexamethasone Differentially Inhibits Thyroxine- or Growth Hormone-Induced Body and Organ Growth of Snell Dwarf Mice

Rooman, Raoul; Kuijpers, Gilliam; Gresnigt, Ria; Bloemen, R. J.; Koster, Johanna G.; Buul-Offers, S. C. van

doi:10.1210/en.2003-0062

Cited by 11 publications

(9 citation statements)

References 44 publications

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“…The combination of Dex+T 4 gave similar results for body length and weight in dwarf mice to those observed in this study [5]. Furthermore, the present data suggest that with respect to body length, treatment for periods longer than one week with T 4 does not improve the final outcome.…”

Section: Discussionsupporting

confidence: 85%

“…With respect to Dex, we have chosen the dose that gave maximal growth retardation in growing mice as published previously [32]. Growth of Snell dwarf mice was maximally stimulated by 1 mg T 4 [5,33].…”

Section: Animals Experimental Design and Tissue Preparationmentioning

confidence: 99%

“…GC treatment, however, results in serious side effects and, especially in children, growth retardation and early onset of osteoporosis develop after long-term treatment [1,2,3]. Today, combination therapies with other hormones are often recommended in order to prevent or diminish these deleterious effects of GCs [4,5,6]. Besides GH, which is already used as an anabolic agent to counteract the effects of GCs [7,8,9,10], PTH and T 4 are important regulators of bone growth too, and these could additionally serve as anabolic agents [5,11,12,13,14].…”

Section: Introductionmentioning

confidence: 99%

“…Today, combination therapies with other hormones are often recommended in order to prevent or diminish these deleterious effects of GCs [4,5,6]. Besides GH, which is already used as an anabolic agent to counteract the effects of GCs [7,8,9,10], PTH and T 4 are important regulators of bone growth too, and these could additionally serve as anabolic agents [5,11,12,13,14]. It has been shown in adult mice that PTH can prevent GC-induced osteoporosis, presumably by blocking osteoblast and osteocyte apoptosis [15].…”

Section: Introductionmentioning

confidence: 99%

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Thyroid hormone, but not parathyroid hormone, partially restores glucocorticoid-induced growth retardation

et al. 2005

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Growth retardation is a serious side effect of long-term glucocorticoid (GC) treatment. In order to prevent or diminish this deleterious effect, a combination therapy including growth hormone (GH), a stimulator of bone growth, is often recommended. Parathyroid hormone (PTH) and thyroid hormone (T(4)) are important hormonal regulators of bone growth, and might also be helpful anabolic agents for counteracting the negative effects of GCs. Therefore, we studied the interaction of GCs in combination with a single dose of either PTH or T(4) on GC-induced growth retardation. Dexamethasone (Dex) treatment of mice for four weeks induced a significant growth inhibition of body length and weight and weights of several organs. PTH or T(4) alone did not affect the normal growth pattern. However, T(4) could partially restore the Dex-induced growth inhibition, whereas PTH could not. Although PTH did not affect total body growth, it did affect the height of the proliferative zone, which could be counteracted by Dex. This contrasts with T(4) treatment alone or in combination with Dex, which both resulted in a disturbed morphology of the growth plate. IGF-I mRNA, one of the mediators of longitudinal bone growth, was present in proliferative and hypertrophic chondrocytes. However, its expression was not affected by any of the treatments. In conclusion, T(4) but not PTH can partially counteract the effects of Dex on general body growth, with possible implications for future treatments of GC-induced growth retardation. Additionally, both T(4) and PTH, alone or in combination with Dex, have differential effects on the morphology of the growth plate.

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Section: Discussionsupporting

confidence: 85%

Section: Animals Experimental Design and Tissue Preparationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Thyroid hormone, but not parathyroid hormone, partially restores glucocorticoid-induced growth retardation

et al. 2005

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“…liver growth observed in response to GH (39,40), because hepatocytes are essentially devoid of IGF-1 receptors (41).…”

Section: Discussionmentioning

confidence: 99%

Growth Hormone–Mediated Janus Associated Kinase–Signal Transducers and Activators of Transcription Signaling in the Growth Hormone–Resistant Potassium-Deficient Rat

Schaefer¹,

Yoon

Nouri

et al. 2004

Journal of the American Society of Nephrology

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Abstract. Potassium deficiency (KD) is associated with severe growth failure, in part caused by growth hormone (GH) resistance. This study set out to determine whether the resistance could be caused by a defect in GH-mediated janus associated kinasesignal transducers and activators of transcription (STAT) signaling as occurs in uremia. To this end, rats were fed a K-deficient diet for 8 d and pair-fed controls received a K-replete diet. Animals from each group received GH or vehicle, and during this period, KD rats were GH resistant; GH induced body and liver weight gain and linear body growth were severely attenuated in these rats. In addition, signal transduction was studied in the liver of rats that were killed 10 or 15 min after an intravenous GH bolus or vehicle. When the rats were killed, GH receptor mRNA and protein levels were similar in the two groups. The abundance of STAT5, STAT3, and STAT1, proteins that mediate GH signaling, was significantly increased by 40 to 130% in KD. Furthermore, GH induced a far greater increase in STAT5 and STAT3 phosphorylation in this group. STAT5 phosphorylation was enhanced fourfold even when normalized for total STAT5 content. Phosphorylated STAT5 and STAT3 proteins were also increased in nuclear extracts, suggesting normal nuclear translocation of the activated signaling proteins. DNA binding of nuclear STAT5 was unaltered. Thus, in KD, there is resistance to the growth-promoting action of GH despite hyperactivation of the janus associated kinase-STAT signaling pathway. This suggests the presence of a defect distal to the nuclear binding of STAT or, alternatively, a defect in a STAT-independent GH-activated signaling pathway.

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Purified proteins from leishmania amastigotes-induced delayed type hypersensitivity reactions and remission of collagen-induced arthritis in animal models

O'Daly¹,

Gleason²,

Sandoval³

et al. 2010

Arch Dermatol Res

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A treatment preparation composed of purified Leishmania (L) antigenic fractions (AS210) induced linear delayed type hypersensitivity (DTH) reactions over a 1-40 microg dose range, in guinea pigs. When a DBA-1 mouse collagen induced arthritis (CIA) model was used to compare AS210 treatment against: a polyvalent vaccine (AS110-1), a monovalent vaccine (AS110-2) and placebo, the AS210 treated mice had the least amount of forepaw inflammation and the lowest mean arthritis scores (MAS). When MAS for day(s) 1-40 were analyzed using one way ANOVA, statistically significant (P < 0.05) differences were seen for the following study groups: PBS versus Dexamethasone and PBS versus AS210. Subsequently, the ANOVA analysis results were corroborated by the Mann-Whitney test: analysis of the first group (P < 0.001) and analysis of the second group (P < 0.001). Comparison between dexamethasone and AS210 at different time intervals by Mann-Whitney test were as follows: day 0-day 5 both treatments had equal values (P = 1.00), from day-7 to 20 AS210 treatment had lower MAS values than dexamethasone (P = 0.037), and from day-21 to 30, AS210 MAS were similar to dexamethasone values (P = 0.319). No statistical difference was observed between AS110-1, AS110-2, and placebo groups.

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Dexamethasone Differentially Inhibits Thyroxine- or Growth Hormone-Induced Body and Organ Growth of Snell Dwarf Mice

Cited by 11 publications

References 44 publications

Thyroid hormone, but not parathyroid hormone, partially restores glucocorticoid-induced growth retardation

Thyroid hormone, but not parathyroid hormone, partially restores glucocorticoid-induced growth retardation

Growth Hormone–Mediated Janus Associated Kinase–Signal Transducers and Activators of Transcription Signaling in the Growth Hormone–Resistant Potassium-Deficient Rat

Purified proteins from leishmania amastigotes-induced delayed type hypersensitivity reactions and remission of collagen-induced arthritis in animal models

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