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Sci Rep. 2016 Jan 27;6:19781. doi: 10.1038/srep19781.

Skeletal muscle Heat shock protein 60 increases after endurance training and induces peroxisome proliferator-activated receptor gamma coactivator 1 α1 expression.

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Department of Experimental Biomedicine and Clinical Neurosciences (BioNeC), University of Palermo, Palermo, 90127 Italy.
Euro-Mediterranean Institute of Science and Technology (IEMEST), Palermo, 90100, Italy.
Department of Anatomical, Histological, Forensic &Orthopaedic Sciences, Section of Histology &Medical Embryology, Sapienza University of Rome, Rome, 00161, Italy.
Interuniversity Institute of Myology, Rome, 00161, Italy.
University Pierre et Marie Curie Paris, UR4 Aging, Stress, Inflammation, 75005 Paris, France.
Department of Microbiology and Immunology, School of Medicine, University of Maryland at Baltimore, IMET, 21201 Baltimore, MD, USA.


Heat shock protein 60 (Hsp60) is a chaperone localizing in skeletal muscle mitochondria, whose role is poorly understood. In the present study, the levels of Hsp60 in fibres of the entire posterior group of hindlimb muscles (gastrocnemius, soleus, and plantaris) were evaluated in mice after completing a 6-week endurance training program. The correlation between Hsp60 levels and the expression of four isoforms of peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC1α) were investigated only in soleus. Short-term overexpression of hsp60, achieved by in vitro plasmid transfection, was then performed to determine whether this chaperone could have a role in the activation of the expression levels of PGC1α isoforms. The levels of Hsp60 protein were fibre-type specific in the posterior muscles and endurance training increased its content in type I muscle fibers. Concomitantly with the increased levels of Hsp60 released in the blood stream of trained mice, mitochondrial copy number and the expression of three isoforms of PGC1α increased. Overexpressing hsp60 in cultured myoblasts induced only the expression of PGC1 1α, suggesting a correlation between Hsp60 overexpression and PGC1 1 α activation.

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