期刊
GROWTH HORMONE & IGF RESEARCH
卷 12, 期 6, 页码 388-398出版社
CHURCHILL LIVINGSTONE
DOI: 10.1016/S1096-6374(02)00079-5
关键词
dwarfism; IL-6; transgenic mice; IGF-I
资金
- NIDCR NIH HHS [1R01 DE10979] Funding Source: Medline
This paper is concerned with growth retardation associated with overproduction of interleukin-6 (IL-6). As a model, we used MUP/hIL-6 transgenic mice in which human IL-6 cDNA is overexpressed under the control of a MUP gene enhancer/promoter. The growth-retardation of MUP/hIL-6 transgenic mice was paralleled by reduced serum levels of IGF-I. As shown, hepatic IGF-I mRNA levels were reduced in the transgenic mice. MUP/hIL-6 transgenic mice are in a state of growth hormone (GH)-resistance, since their serum GH levels are either normal or elevated. To identify possible steps in GH signaling which might be perturbed in the transgenic mice, we examined the synthesis of GH receptor (GHR) mRNA. We noted a twofold reduction of hepatic GHR mRNA in the transgenic mice. We therefore conclude that overexpression of IL-6 brings about growth impairment in part through a GH receptor defect. (C) 2002 Elsevier Science Ltd. All rights reserved.
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