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Acta Physiologica Congress

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Acta Physiologica 2011; Volume 203, Supplement 688
The 62nd National Congress of the Italian Physiological Society
9/25/2011-9/27/2011
Sorrento, Italy


THE TIME COURSE OF DISUSE ATROPHY IN A SLOW AND FAST MUSCLE OF HINDLIMB UNLOADED MICE
Abstract number: O15

CANNAVINO1 J, BROCCA1 L, DESAPHY2 JF, SANDRI3 M, CONTE CAMERINO2 D, PELLEGRINO1 MA, BOTTINELLI1 R

1Dept of Physiology, Pavia, Italy
2Dept of Pharmaco-Biology, Pharmacology Unit, Univ. of Bari, Bari, Italy
3Dulbecco Telethon Institute at Venetian Institute of Molecular Medicine, Padova, Italy

In order to understand the mechanisms underlying disuse atrophy we studied the adaptation of slow and fast muscles (soleus and gastrocnemius) at different time of suspension (3 and 7 days). Morphological analysis of gastrocnemius muscle showed a similar decrease of CSA fiber (18%) at 3 and 7 days of suspension. We found an up-regulation in gene expression of autophagy system (P62), ubiquitin-proteasome system (Murf1), and oxidative stress (Nrf1, Mt1) at 3 days; we showed also an up-regulation in protein involved in antioxidant defense systems (SOD1, Catalase and Hsp70) at 3 and 7 days. Markers of oxidative and glycolitic metabolism were also studied, but they were unchanged. Soleus muscle showed 1 type fiber atrophy only at 7 days (9%), whereas type 2A muscle fibers atrophy was found at 3 (6%) and at 7 days (14%). Gene expression analysis of soleus showed an up-regulation of ubiquitin-proteasome system (Murf1), oxidative stress (Nrf1, Mt1) and mitochondrial biogenesis (TFAM) at 3 days and showed an unchanged expression of the main coordinator of oxidative metabolism (PGC1a). In a previous study we demonstrated that soleus muscle was characterized by metabolic impairment after 14 days of suspension. Further experiments are ongoing to clarify the relative role of oxidative stress and metabolic impairment following HU and will be presented at the meeting.

To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 203, Supplement 688 :O15

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