Abstract
Mice lacking suppressor of cytokine signaling-2 (SOCS-2) exhibit accelerated postnatal growth resulting in adult mice that are 1.3 to 1.5 times the size of normal mice. In this study we examined the somatotrophic pathway to determine whether the production or actions of GH or IGF-I are altered in these mice. We demonstrated that SOCS-2(-/-) mice do not have elevated GH levels and suffer no major pituitary dysmorphogenesis, and that SOCS-2-deficient embryonic fibroblasts do not have altered IGF-I signaling. Primary hepatocytes from SOCS-2(-/-) mice, however, did have moderately prolonged signal transducer and activator of transcription 5 signaling in response to GH stimulation. Furthermore, the deletion of SOCS-2 from mice also lacking signal transducer and activator of transcription 5b had little effect on growth, suggesting that the action of SOCS-2 may be the regulation of the GH signaling pathway.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Blotting, Western
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Body Weight / drug effects
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Cell Line
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DNA-Binding Proteins / metabolism*
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Female
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Gene Deletion
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Growth / drug effects
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Growth Hormone / metabolism
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Growth Hormone / pharmacology
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Hepatocytes / drug effects
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Hepatocytes / metabolism
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Insulin-Like Growth Factor I / pharmacology
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Male
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Mice
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Mice, Knockout
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Milk Proteins*
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Phosphorylation
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Pituitary Gland / metabolism
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Pituitary Gland / pathology
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Proteins / genetics
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Proteins / metabolism*
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RNA, Messenger / genetics
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RNA, Messenger / metabolism
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Repressor Proteins*
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STAT5 Transcription Factor
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Signal Transduction / drug effects
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Skin / pathology
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Suppressor of Cytokine Signaling Proteins
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Trans-Activators / metabolism*
Substances
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DNA-Binding Proteins
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Milk Proteins
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Proteins
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RNA, Messenger
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Repressor Proteins
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STAT5 Transcription Factor
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Socs2 protein, mouse
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Stat5b protein, mouse
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Suppressor of Cytokine Signaling Proteins
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Trans-Activators
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Insulin-Like Growth Factor I
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Growth Hormone