α-linolenic acid reduces TNF-induced apoptosis in C2C12 myoblasts by regulating expression of apoptotic proteins

  • Felicia Carotenuto Department Clinical Sciences and Translational Medicine, University of Rome Tor Vergata, Rome; Diagnostics and Metrology Laboratory, FSN-TECFIS-DIM, ENEA-Frascati, Rome, Italy.
  • Dario Coletti Department of Biological Adaptation and Aging B2A, University Pierre et Marie Curie Paris 06, Paris, France; Section of Histology and Medical Embryology, Department of Anatomical, Histological, Forensic and Orthopaedic Sciences, Sapienza University of Rome, Italy.
  • Paolo Di Nardo Department Clinical Sciences and Translational Medicine, University of Rome Tor Vergata, Rome, Italy.
  • Laura Teodori | laura.teodori@enea.it Diagnostics and Metrology Laboratory, FSN-TECFIS-DIM, ENEA-Frascati, Rome, Italy.

Abstract

Impaired regeneration and consequent muscle wasting is a major feature of muscle degenerative diseases. Nutritional interventions as adjuvant strategy for preventing such conditions are recently gaining increasing attention. Ingestion of n3-polyunsaturated fatty acids has been suggested to have a positive impact on muscle diseases. We recently demonstrated that the dietary n3-fatty acid, alpha-linolenic acid (ALA), exerts potent beneficial effects in preserving skeletal muscle regeneration in models of muscle dystrophy. To better elucidate the underlying mechanism we investigate here on the expression level of the anti- and pro-apototic proteins, as well as caspase-3 activity, in C2C12 myoblasts challenged with pathological levels of TNF. The results demonstrated that ALA protective effect on C2C12 myoblasts was associated to an increased Bcl-2/Bax ratio. Indeed, the effect of ALA was directed to rescue Bcl-2 expression and decrease Bax expression both affected in an opposite way by TNF treatment. This effect was associated with a decrease in caspase-3 activity by ALA. TNF is a major pro-inflammatory cytokine that is expressed in damaged skeletal muscle, therefore, counteract inflammatory signals in the muscle microenvironment represents a critical strategy to ameliorate skeletal muscle pathologies

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Author Biographies

Felicia Carotenuto, Department Clinical Sciences and Translational Medicine, University of Rome Tor Vergata, Rome; Diagnostics and Metrology Laboratory, FSN-TECFIS-DIM, ENEA-Frascati, Rome
Department Clinical Sciences and Translational Medicine
Dario Coletti, Department of Biological Adaptation and Aging B2A, University Pierre et Marie Curie Paris 06, Paris, France; Section of Histology and Medical Embryology, Department of Anatomical, Histological, Forensic and Orthopaedic Sciences, Sapienza University of Rome
Department of Biological Adaptation and Aging B2A
Paolo Di Nardo, Department Clinical Sciences and Translational Medicine, University of Rome Tor Vergata, Rome
Department Clinical Sciences and Translational Medicine
Laura Teodori, Diagnostics and Metrology Laboratory, FSN-TECFIS-DIM, ENEA-Frascati, Rome
Diagnostics and Metrology Laboratory, FSN-TECFIS-DIM
Published
2016-12-15
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Section
Myology Made in Italy
Keywords:
Myoblasts, Apoptotic proteins, Muscle wasting, Inflammation, Phytochemicals
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How to Cite
Carotenuto, F., Coletti, D., Di Nardo, P., & Teodori, L. (2016). α-linolenic acid reduces TNF-induced apoptosis in C2C12 myoblasts by regulating expression of apoptotic proteins. European Journal of Translational Myology, 26(4). https://doi.org/10.4081/ejtm.2016.6033