Insulin-like Growth Factor I (Igf-i) and Its Receptor (Igf-1r) in the Rat Anterior Pituitary.
From: Division of Neuroendocrinology, Institute of Anatomy, University of Zürich, Winterthurerstr. 190, CH-8057 Zürich, Switzerland.
The European journal of neuroscience
- Publish Date: Jan 2007
- ISSN: 0953-816X
- Volume: 25
- Issue: 1
- Pages: 191-200
- Medium: Print
- Language: English
- Citation (JAMA): Eppler Elisabeth, Jevdjovic Tanja, Maake Caroline, et al. Insulin-like Growth Factor I (Igf-i) and Its Receptor (Igf-1r) in the Rat Anterior Pituitary.. Eur. J. Neurosci. Jan 2007;25:191-200
Abstract
Few and controversial results exist on the cellular sites of insulin-like growth factor (IGF)-I synthesis and the type 1 IGF receptor (IGF-1R) in mammalian anterior pituitary. Thus, the present study analysed IGF-I and the IGF-1R in rat pituitary. Reverse transcription-polymerase chain reaction revealed IGF-I and IGF-1R mRNA expression in pituitary. The sequences of both were identical to the corresponding sequences in other rat organs. In situ hybridization localized IGF-I mRNA in endocrine cells. The majority of the growth hormone (GH) cells and numerous adrenocorticotropic hormone (ACTH) cells exhibited IGF-1R-immunoreactivity at the cell membrane. At lower densities, IGF-1 receptors were also present at the other hormone-producing cell types, indicating a physiological impact of IGF-I for all endocrine cells. IGF-I-immunoreactivity was located constantly in almost all ACTH-immunoreactive cells. At the ultrastructural level, IGF-I-immunoreactivity was confined to secretory granules in co-existence with ACTH-immunoreactivity, indicating a concomitant release of both hormones. Occasionally, IGF-I-immunoreactivity was detected in an interindividually varying number of GH cells. In some individuals, weak IGF-I-immunoreactions were also detected also in follicle-stimulating hormone and luteinizing hormone cells. Thus, IGF-I seems to be produced as a constituent in ACTH cells, possibly indicating its particular importance in stress response. Generally, IGF-I from the endocrine cells may regulate synthesis and/or release of hormones in an autocrine/paracrine manner as well as prevent apoptosis and stimulate proliferation. Production of IGF-I in GH cells may depend on the physiological status, most likely the serum IGF-I level. IGF-I released from GH cells may suppress GH synthesis and/or release by an autocrine feedback mechanism in addition to the endocrine route.
Mesh Headings (Keywords): Adrenocorticotropic Hormone, Animals, Female, Gene Expression, Immunohistochemistry, In Situ Hybridization, Insulin-Like Growth Factor I, Male, Microscopy, Immunoelectron, Pituitary Gland, Anterior, RNA, Messenger, Rats, Rats, Wistar, Receptor, IGF Type 1, Reverse Transcriptase Polymerase Chain Reaction, Sex Factors
Check for Full Text / PubMed Unique Identifier (PMID): 17241280
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