Thyroxine and triiodothyronine levels in Snell mice

Buul‐Offers, Sylvia van; Hackeng, W. H. L.; Schopman, W.

doi:10.1530/acta.0.1020396

Cited by 19 publications

(11 citation statements)

References 20 publications

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“…Moreover, several reports indicate a deficiency in thyroid-stimulating hormone production of thyroxine in the Snell dwarf mice. 49,50 It is particularly interesting that tyroxine is required for proliferation of marrow B cells, 51 and also acts directly on growth plate chondrocytes to promote hypertrophy. 52 We are thus looking into the possibility that the Snell-Bagg dwarf mice represent an animal model with defects affecting the same cascade of interacting molecules as that altered in the collagen X mice.…”

Section: Discussionmentioning

confidence: 99%

Linking Hematopoiesis to Endochondral Skeletogenesis through Analysis of Mice Transgenic for Collagen X

Jacenko

Roberts

Campbell

et al. 2002

The American Journal of Pathology

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The vertebrate skeleton forms predominantly by endochondral ossification (EO), where the cartilaginous model of the axial and appendicular skeleton, as well as of certain cranial bones, is replaced by bony trabeculae and marrow. The distinctive feature of this process is comprised of hypertrophic cartilage where EO initiates and collagen X is predominant.1 Emergence of hypertrophic cartilage defines each skeletal element where marrow forms. Since the marrow provides niches for blood cell differentiation, alterations in the cartilage-to-bone and marrow transition of EO may affect stromal and hematopoietic constituents. We demonstrate here that mice transgenic (Tg) for collagen X develop both skeletal and hematopoietic abnormalities, and that the latter likely arise as a consequence of disrupted collagen X function. These data reveal an unforeseen link between endochondral skeletogenesis and establishment of the marrow microenvironment prerequisite for hematopoiesis.During embryogenesis, EO initiates in cartilage with hypertrophy, and progresses by transforming a preexisting non-calcified avascular cartilage to a calcifiable one permissive to vascularization.

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Section: Discussionmentioning

confidence: 99%

Linking Hematopoiesis to Endochondral Skeletogenesis through Analysis of Mice Transgenic for Collagen X

Jacenko

Roberts

Campbell

et al. 2002

The American Journal of Pathology

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“…The deficient TSH status of the Snell mutant has been based largely on the failure to detect thyrotrophs in the anterior pituitary (Roux et al 1982), the failure of thyrotrophichormone-releasing hormone (TRH) to elicit a rise in plasma TSH (Roti, Christianson, Harris, Braverman & Vagenakis, 1978) and estimations of thyroid activity both physiologically and ultrastructurally (Howe, Howe & Pollard, 1980;Van Buul-Offers, Hackeng The exact aetiology of the condition remains unknown. Although a hypothalamic defect controlling growth-hormone production seems ruled out by the experiment of Garsner & Rennels (1960), a deficiency in hypothalamic dopamine may explain the prolactin deficiency (Morgan, Bartke & Pfeil, 1981).…”

Section: The Snell Dwarf Mousementioning

confidence: 99%

Mouse Mutants as Models in Endocrine Research

Charlton

1984

Exp Physiol

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Although Shire (1979) has listed some forty‐eight mouse mutants of interest to the endocrinologist, this short review has concentrated upon eleven mutations which have resulted in a significant number of scientific publications over the last 4 or 5 years. The selection of references has had to be limited, but it should be possible easily to expand the list given in this review. Although the proximate cause of none of the eleven mutations has been identified with certainty, the abnormalities of function have included hormone deficiencies and receptor and post‐receptor malfunctions. It is perhaps a reflexion on our society in the 1980s, that the bulk of research has concentrated on the obese mouse. However, we still do not know the initial cause of this syndrome. The major disadvantage of the mouse to the hormone assayist lies in the small blood volume and the extreme difficulty in taking serial blood samples over a short period of time. With increased sophistication of assay techniques this may prove less daunting, but is an area where a review of the literature reveals discrepancies between laboratories, and even between data generated by the same laboratory at different times. With regard to the hormone content of endocrine tissues, the way forward for peptide‐secreting glands may be in the measurement of mRNA levels for particular hormones. Certainly the methods of recombinant‐DNA technology will yield positive information upon the aetiology and expression of some of the syndromes considered above. Organ transplantation is an area in which mutant mice have proved useful, for example gonadal, pituitary and pancreatic tissue transplantation. The grafting of neural tissue in the hpg mouse has added a further dimension to this field of research. The great infrastructure of genetical research in mice has enabled us to breed mutant genes onto different genetic backgrounds. This area of research is one which deserves to expand. The techniues of in vitro fertilization, chimera formation and embryo transfer have been used, in part, in studies on mouse mutants, and should provide technical means for further investigating gene expression. The family of dwarf mutants are ideally suited for research into the expression of genes micro‐injected into the fertilized egg (see Charlton & Cox, 1983). As new hormones are isolated and become available for study these mouse mutants may well be useful in delineating physiological functions for natural and pharmacological products. Again, the dwarf mutants would seem ideally suited for research into the synthesis and action of GRF. Mouse mutants have proved of use to biochemists and embryologists and provide fertile ground for endocrine investigations ranging from molecular genetics to membrane biophysics.

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“…Up to now, this phenomenon, namely an increase in testis weight with advanced age , has not been observed in dwarf mice [6] or dwarf rats [1,3] with pituitary GH deficiency. Since the rdw rat is characterized by GH and PRL deficiency, it is interesting to speculate whether PRL deficiency is related to the increase in testis weight and the appearance of edema in the testis.…”

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confidence: 95%