Regulation of Components of the Ubiquitin System by Insulin-Like Growth Factor I and Growth Hormone in Skeletal Muscle of Rats Made Catabolic with Dexamethasone
Dionisios Chrysis, Louis E. Underwood
Abstract
Dionisios Chrysis, Louis E. Underwood
Abstract
To investigate whether the anabolic effects of insulin-like growth factor I (IGF-I) and GH are mediated through regulation of the ubiquitin (Ub) pathway, we examined the effect of IGF-I (0.35 microg/100 g) and/or GH (0.3 mg/100 g BW) on the expression of Ub and Ub-conjugating (E2) enzyme messenger RNAs (mRNAs) in skeletal muscle of rats made catabolic by treatment with dexamethasone (Dex; 0.5 mg/100 g BW) for 3 days. Dex caused a significant loss of body and gastrocnemius weight (14% and 25%, respectively) concurrent with an increase in the 2.8- and 1.2-kb transcripts of Ub (14.3- and 12-fold increases, respectively), the 1.8- and 1.2-kb transcripts of 14-kDa Ub-conjugating enzyme (E2-14 kDa; 5.6- and 7.7-fold increases, respectively), the 4.4- and 2.4-kb transcripts of Ub-E2G (6.5- and 8.2-fold increases, respectively), and the 2E isoform of the 17-kDa E2 mRNA (3.5-fold increase). Injections of IGF-I in Dex-treated animals ameliorated the body weight loss, and the gastrocnemius tended to be heavier. This improvement was also accompanied by a significant suppression of transcripts for Ub (58% and 66% decreases), E2-14 kDa (58% and 68% decreases), and Ub-E2G (78% decrease), whereas the 2E isoform of the 17-kDa E2 was only modestly affected (20% decrease). GH restored serum IGF-I levels to normal in Dex-treated rats, but had no effect on the body weight loss or on any of the studied components of the Ub pathway. Administration of IGF-I to the Dex/GH-treated animals decreased the activated mRNAs of the Ub pathway in a manner and degree similar to those observed in the Dex/ IGF-I group. In summary, these results provide evidence that IGF-I regulates the expression of mRNAs encoding components of the Ub pathway during catabolism and suggest a possible mechanism for the antiproteolytic actions of IGF-I. On the other hand, GH, which is believed not to affect proteolysis but only protein synthesis, had no effect on any of the mRNAs studied.
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To investigate whether the anabolic effects of insulin-like growth factor I (IGF-I) and GH are mediated through regulation of the ubiquitin (Ub) pathway, we examined the effect of IGF-I (0.35 microg/100 g) and/or GH (0.3 mg/100 g BW) on the expression of Ub and Ub-conjugating (E2) enzyme messenger RNAs (mRNAs) in skeletal muscle of rats made catabolic by treatment with dexamethasone (Dex; 0.5 mg/100 g BW) for 3 days. Dex caused a significant loss of body and gastrocnemius weight (14% and 25%, respectively) concurrent with an increase in the 2.8- and 1.2-kb transcripts of Ub (14.3- and 12-fold increases, respectively), the 1.8- and 1.2-kb transcripts of 14-kDa Ub-conjugating enzyme (E2-14 kDa; 5.6- and 7.7-fold increases, respectively), the 4.4- and 2.4-kb transcripts of Ub-E2G (6.5- and 8.2-fold increases, respectively), and the 2E isoform of the 17-kDa E2 mRNA (3.5-fold increase). Injections of IGF-I in Dex-treated animals ameliorated the body weight loss, and the gastrocnemius tended to be heavier. This improvement was also accompanied by a significant suppression of transcripts for Ub (58% and 66% decreases), E2-14 kDa (58% and 68% decreases), and Ub-E2G (78% decrease), whereas the 2E isoform of the 17-kDa E2 was only modestly affected (20% decrease). GH restored serum IGF-I levels to normal in Dex-treated rats, but had no effect on the body weight loss or on any of the studied components of the Ub pathway. Administration of IGF-I to the Dex/GH-treated animals decreased the activated mRNAs of the Ub pathway in a manner and degree similar to those observed in the Dex/ IGF-I group. In summary, these results provide evidence that IGF-I regulates the expression of mRNAs encoding components of the Ub pathway during catabolism and suggest a possible mechanism for the antiproteolytic actions of IGF-I. On the other hand, GH, which is believed not to affect proteolysis but only protein synthesis, had no effect on any of the mRNAs studied.
Key concepts: Internal medicine, Endocrinology, Anabolism, Insulin-like growth factor, Skeletal muscle, Catabolism, Growth factor, Dexamethasone