Growth and differentiation in the rat following hypophysectomy at 6 days of age

Walker, Donald G.; Simpson, Miriam E.; Asling, C. Willet; Evans, Herbert M.

doi:10.1002/ar.1091060403

Cited by 102 publications

(34 citation statements)

References 7 publications

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“…GH-deficient mice have normal birth weights (20,21), and rats hypophysectomized 6 days after birth grow normally for 2 weeks (22). Analysis of transgenic GH mice supports these data, because these mice do not manifest accelerated growth relative to that of control littermates until approximately 3 weeks postpartum (5).…”

Section: Discussionmentioning

confidence: 86%

Expression of Insulin-Like Growth Factor I in Transgenic Mice with Elevated Levels of Growth Hormone Is Correlated with Growth*

et al. 1988

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To study the role of insulin-like growth factor I (IGF-I) in mediating the growth-promoting function of GH, IGF-I expression was assayed in transgenic mice carrying either GH or GRF fusion genes. These mice exhibit enhanced growth as a result of high level ectopic expression of GH and have 2-fold elevation of both hepatic IGF-I mRNA levels and circulating IGF-I levels. Hepatic IGF-I mRNA levels are low at birth regardless of GH levels; they increase approximately 10-fold during postnatal development and become GH inducible 2 weeks after birth. The ontogeny of circulating IGF-I is similar. Accelerated growth in transgenic mice with GH fusion genes commences 3 weeks after birth despite high circulating GH levels at least as early as birth. In addition, endogenous mouse GH-secreting somatotroph cells in the pituitary are present in normal numbers at 3 weeks, but are undetectable 4 weeks after birth. Because the time at which IGF-I expression becomes GH responsive slightly precedes both the initiation of accelerated growth and the time when endogenous GH disappears, we conclude that IGF-I is directly involved in mediating the GH signal and that delayed induction of IGF-I gene expression is responsible, at least in part, for the delayed onset of other GH-responsive events.

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Section: Discussionmentioning

confidence: 86%

Expression of Insulin-Like Growth Factor I in Transgenic Mice with Elevated Levels of Growth Hormone Is Correlated with Growth*

et al. 1988

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“…Genetically GH-deficient animals (8) and hypophysectomized neonates (1) grow normally for the first 2 weeks after birth. Similarly, transgenic animals overexpressing hGH or IGF-1 also grow normally until 2 to 4 weeks of age (21,37). There is some evidence to suggest that the induction of IGF-1 in the liver by GH is developmentally regulated (36); whether or not this applies to other sites of IGF-1 synthesis is open to question.…”

Section: Discussionmentioning

confidence: 99%

Osteoblast-specific expression of growth hormone stimulates bone growth in transgenic mice.

Baker¹,

Hollingshead²,

Pitts-Meek³

et al. 1992

Mol. Cell. Biol.

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Growth hormone (GH) is an important regulator of postnatal growth, acting on a wide variety of target tissues. Here, we show that local production of GH in osteoblasts is able to stimulate bone growth directly without significant systemic effects. Mice were made transgenic by microinjection of an osteocalcin-human GH (osteocalcin-hGH) gene construct in which approximately 1,800 bp of the rat osteocalcin promoter was fused to the hGH gene. Five lines of transgenic mice, each with measurable amounts of serum hGH (ranging from 1 to 1,000 ng/ml), were analyzed. Northern (RNA) blot hybridization showed that the hGH transcript was detectable only in the bone. Further characterization of hGH mRNA distribution by in situ hybridization revealed that in neonates the most intense signal was found in periosteal osteoblasts and in odontoblasts, while in adults, trabecular and endosteal osteoblasts were favored. In one transgenic line (992-1), hGH was expressed at a much lower level and had minimal systemic effects; however, the local concentrations of hGH in bone were sufficient to stimulate bone growth in these animals.

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“…The pattern of growth observed is consistent with data on the role of GH during early postnatal growth. Both GH-deficient mice and hypophysectomized rats grow at approximately normal rates for 2 weeks after birth (Walker et al 1950;Eicher and Beamer 1976). In addition, transgenic mice harboring foreign GH genes expressing high levels of GH do not show accelerated growth rates until 3 weeks after birth (Palmiter et al 1982Hammer et al 1984).…”

Section: Dt-a Casselle Rgh-hghmentioning

confidence: 99%

Dwarf mice produced by genetic ablation of growth hormone-expressing cells.

Behringer¹,

Mathews²,

Palmiter³

et al. 1988

Genes Dev.

317

124

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Fusion of the 310 bp located 5' of the rat growth hormone (GH) gene to the human GH structural gene resulted in somatotrope-specific expression in transgenic mice. Human GH transcripts were detected only in pituitaries of these mice, and immunocytochemical analyses revealed that this expression was limited to GH-expressing cell types. The rat GH 5' sequences were then used to direct the expression of diphtheria toxin to the GHexpressing cells of transgenic mice. A line of mice was established which lacks detectable levels of circulating GH. This deficiency resulted in dwarfism; transgenic animals grew only to half the size of nontransgenic littermates. Nearly all somatotropes were absent, as shown by GH immunostaining in the transgenic pituitaries. Prolactin (PRL)-producing lactotropes, thought to share a common cellular origin with somatotropes, were also reduced in numbers. A model for the lineal relationships between GH-and PRLsynthesizing cells is proposed.

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Growth and differentiation in the rat following hypophysectomy at 6 days of age

Cited by 102 publications

References 7 publications

Expression of Insulin-Like Growth Factor I in Transgenic Mice with Elevated Levels of Growth Hormone Is Correlated with Growth*

Expression of Insulin-Like Growth Factor I in Transgenic Mice with Elevated Levels of Growth Hormone Is Correlated with Growth*

Osteoblast-specific expression of growth hormone stimulates bone growth in transgenic mice.

Dwarf mice produced by genetic ablation of growth hormone-expressing cells.

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