Abstracts of the 7th Cachexia Conference, Kobe/Osaka, Japan, December 9–11, 2013

s of the 7th Cachexia Conference, Kobe/Osaka, Japan, December 9–11, 2013 Published online: 5 November 2013 # Springer-Verlag Berlin Heidelberg 2013 1–01 Regeneration of the rat tibialis anteriormuscle is impaired despite induction of the SPARC-beta-catenin pathway during post-immobilization recovery Lamia Slimani, Emilie Vazeille , Christiane Deval , Julien Amat, Cécile Polge, Daniel Béchet , Daniel Taillandier , Dominique Dardevet , Lydie Combaret , Didier Attaix INRA, UMR 1019, CRNH Auvergne, Clermont Université, Clermont-Ferrand, France, Centre Hospitalier Universitaire, Clermont-Ferrand, France Background and aims: The immobilization-induced tibialis anterior (TA) muscle atrophy worsens after cast removal concomitantly with changes in the extracellular matrix composition. SPARC is a matricellular glycoprotein involved in tissue response to injury and in stabilization ofƒnbeta-catenin, which induces muscle regulatory factors (MRFs) controlling muscle regeneration. We hypothesized that SPARC expression changed upon immobilization and could be involved in the worsening of TA muscle atrophy by altering muscle regeneration processes pending cast removal. Methods: Wistar rats were subjected to hindlimb immobilization for 8 days (I8) or not (I0), and allowed to recover for 1 to 10 days (R1-10). Expression of SPARC, beta-catenin, and proliferative (i.e. MyoD and MyF5) or differentiation (i.e. myogenin) MRFs were assessed by Western blots and/or RTqPCR during recovery of previously immobilized TA. Results: SPARC mRNA levels increased only during recovery at R1 (+161 %) and R10 (+200 %), compared to I8 and I0. betacateninmRNA levels increased at I8 (+80%) andR10 (+190%), while protein levels accumulated from R1 to R10 (+350 to 400 %) in immobilized TA vs. I0. MyoD and MyF5 mRNA levels increased by 2–3 fold only at I8 andR1 in immobilized TA vs. I0. By contrast, myogenin mRNA levels decreased at I8 (−60 %) and R1 (−90 %), and increased at R10 (+100 %). Conclusions: We report an induction of the SPARC-betacatenin pathway associated with increased mRNAs of the proliferative MRFs (Myf5 and MyoD) in the recovering TA early after cast removal. The differentiation MRF myogenin was first largely repressed, but increased later on, when TA started to recover. Altogether, the data suggest that the TA tended to preserve muscle regeneration potential through induction of proliferative MRFs. However this process was poorly efficient presumably because of an alteration in satellite cell differentiation. 1–02 Upregulation of genes involved in muscle protein breakdown coincides with downregulation of genes involved in the immunoproteasome in a cancer cachectic C26 mouse model Jvalini T. Dwarkasing, Marlies de Ligt, Francina J. Dijk 2 , Jeroen van Bergenhenegouwen 2 , Mark V Boekschoten , Josep M. Argilès , Yvette Luiking , Alessandro Laviano, Renger F. Witkamp, Klaske van Norren Nutrition and Pharmacology Group, Division of Human Nutrition, Wageningen University, Wageningen, Nutricia Research, Utrecht, The Netherlands, Nutricia Research, Utrecht, The Netherlands, Nutrition, Metabolism and Genomics Group, Division of Human Nutrition, Wageningen University, Wageningen, The Netherlands, Cancer Research Group, Departament de Bioquímica i Biologia Molecular, University of Barcelona, Barcelona, Spain, Department of Clinical Medicine, Sapienza University, Rome, Italy Background: Cachexia is characterized by loss of muscle mass and is associated with complications like a reduced immune response. In cancer patients with low level of immunoproteasome expression, tumour-and infectionderived epitopes have been suggested to have a higher chance of escaping from immune surveillance. Here we present the C26 adenocarcinoma mouse model derived data on transcriptomics analysis of two highly interconnected systems: the muscle protein breakdown, ubiquitinproteasome and the immunoproteasome pathways. Methods: Male CD2F1 mice, aged 5–6 weeks, were randomly divided into a control (C) or a tumour-bearing group J Cachexia Sarcopenia Muscle (2013) 4:295–343 DOI 10.1007/s13539-013-0123-9