Journal article

Muscle-specific deletion of SOCS3 does not reduce the anabolic response to leucine in a mouse model of acute inflammation

MK Caldow, DJ Ham, A Chee, J Trieu, T Naim, DI Stapleton, K Swiderski, GS Lynch, R Koopman

Cytokine | ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD | Published : 2017

Abstract

Excessive inflammation reduces skeletal muscle protein synthesis leading to wasting and weakness. The janus kinase/signal transducers and activators of transcription-3 (JAK/STAT3) pathway is important for the regulation of inflammatory signaling. As such, suppressor of cytokine signaling-3 (SOCS3), the negative regulator of JAK/STAT signaling, is thought to be important in the control of muscle homeostasis. We hypothesized that muscle-specific deletion of SOCS3 would impair the anabolic response to leucine during an inflammatory insult. Twelve week old (n = 8 per group) SOCS3 muscle-specific knockout mice (SOCS3-MKO) and littermate controls (WT) were injected with lipopolysaccharide (LPS, 1 ..

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Grants

Awarded by Australian Research Council


Funding Acknowledgements

This work was supported by the Australian Research Council (ARC; DP120101494). MKC was supported by a McKenzie Research Fellowship from the University of Melbourne. KS was supported by an Early Career Fellowship from the National Health and Medical Research Council (NH & MRC) of Australia.