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Search for other papers by R. J. DUQUESNOY in
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The capacity of specific antisera against growth hormone (GH) to inhibit the biological activity of this hormone has been previously described. Most experiments were carried out on hypophysectomized rats, and the biological activity of GH in the tibia assay could be neutralized by its specific antiserum or crossreacting antisera (Hayashida & Contopoulos, 1967), or by anti-pituitary serum (Anigstein, Rennels & Anigstein, 1960). Pierpaoli & Sorkin (1967, 1968) observed considerable impairment of body growth, often manifested as a runting syndrome, and extensive degeneration of lymphoid tissues after administration of antisera to pituitary extracts of bovine GH to young mice.
The purpose of this study was to investigate the effect of specific antibodies to rat GH (RGH) on young rats. Special attention was paid to the morphology and function of the lymphoid system. Because the thymus plays an important role in development of the lymphoid system early in life, newborn rats were
Search for other papers by A. F. Bristow in
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Search for other papers by R. E. Gaines Das in
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ABSTRACT
Three preparations of recombinant DNA-derived insulin-like growth factor-I (IGF-I) were obtained, prepared in ampoules coded 86/522, 86/720 or 87/518, and evaluated as candidate International Reference Reagents in an international collaborative study (nine laboratories in four countries) in response to a request by the World Health Organization (WHO).
Immunoassay dose–response curves for each of the three preparations did not in general differ significantly from those of local standards or from those of ampouled preparations of serum-derived IGF-I which were included in the study. The estimates of ampoule contents in terms of local standards showed considerable heterogeneity; the between-laboratory variability of estimates in terms of local standards was ten times greater than the inherent variability of estimates from these systems as estimated from comparisons of coded duplicates. Bioassay data were limited, and those available were inconsistent with immunoassay data. Of the three preparations, ampoules coded 86/720 were derived from an IGF-I preparation that was heterogeneous by high-performance liquid chromatography, and stability data for the preparation 86/522 were anomalous.
As a result, the ampouled preparation coded 87/518 has been established by WHO as the International Reference Reagent for IGF-I for immunoassay, with an assigned ampoule content of 3·1 μg/ampoule, and is available from the National Institute for Biological Standards and Control.
Journal of Endocrinology (1990) 125, 191–197
Search for other papers by MR Kritzik in
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Search for other papers by N Sarvetnick in
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We have characterized expression of the ErbB receptor family and one of its ligands, heregulin, in an effort to identify molecules associated with pancreatic development and regeneration. In addition to studying expression during fetal pancreatic development, we have also studied expression during pancreatic regeneration in the interferon-gamma (IFNgamma)-transgenic mouse, which exhibits significant duct cell proliferation and new islet formation. These studies demonstrate significant expression of the ErbB2, ErbB3, and ErbB4 receptors, in addition to heregulin isoforms, in the developing murine fetal pancreas. We also report significant ductal expression of these proteins during IFNgamma-mediated pancreatic regeneration. This striking expression was absent in 1-week-old neonates, but was clearly visible in pups by 5 weeks of age. These data therefore indicate that ErbB receptor and ligand expression decline by birth in both the IFNbeta-transgenic and non-transgenic mice, and that expression resumes early in postnatal life in the IFNbeta-transgenic mice. The expression of ErbB receptor family members at sites of islet development and regrowth suggests that these molecules might be relevant to these processes.
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Search for other papers by N Sarvetnick in
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We have observed pancreatic duct cell proliferation and islet regeneration in transgenic mice whose pancreata produce interferon gamma (IFNg mice). We have previously demonstrated that new islet cells derive from endocrine progenitor cells in the pancreatic ducts of this model. The current study was initiated to define these endocrine progenitor cells further and to identify novel markers associated with pancreatic regeneration. Importantly, we have found that PDX-1, a transcription factor required for insulin gene transcription as well as for pancreatic development during embryogenesis, is expressed in the duct cells of IFNg mice. This striking observation suggests an important role for PDX-1 in the marked regeneration observed in IFNg mice, paralleling its critical function during ontogeny. Also demonstrated was elevated expression of the homeobox-containing protein Msx-2 in the pancreata of fetal mice as well as in adult IFNg mice, identifying this molecule as a novel marker associated with pancreatic development and regeneration as well. The identification of PDX-1 and Msx in the ducts of the IFNg transgenic pancreas but not in the ducts of the non-transgenic pancreas suggests that these molecules are associated with endocrine precursor cells in the ducts of the IFNg transgenic mouse.
