Roberta Di Pietro

Roberta Di Pietro

G. d'Annunzio University of Chieti-Pescara, Italy

Title: Involvement of the caspase enzymes in satellite cells apoptosis


Roberta Di Pietro got the degree in Medicine with Honours in 1985 and PhD in Sports Medicine with Honours in 1988, University of Chieti, Italy. She worked as a visiting Scientist in UK at the Biochemistry Department, AFRC, Cambridge, USA, at the Pathology Department, USUHS, Bethesda and at the Institute of Human Virology, University of Maryland at Baltimore. She currently works at the G. d´Annunzio University of Chieti, Italy, as a Full Professor of Histology. In 2007, she joined the Editorial Board of Current Pharmaceutical Design as an Executive Guest Editor and since 2010 she was recognized as a Registered Referee for Archives of Ophthalmological Reviews and Reproductive Biology and Endocrinology. She is now author of 157 scientific publications plus international e-book and Italian textbook chapters.


Ageing is characterized by an impairment of muscle regenerative potential and a progressive loss of skeletal muscle. This condition, called sarcopenia, has important health care implications for humans, as it contributes to frailty, functional loss and premature death. The ability of skeletal muscle to regenerate is owed to a population of myogenic stem cells called satellite cells (SCs). In previous papers of the research group an age-related decrease in the antioxidant capacity of human SCs that may negatively affect the ageing SCs ability to repair muscle was demonstrated. Despite the involvement of caspases in muscle wasting, the real role of these enzymes is still controversial. To test the possibility of caspases involvement in SCs death in human ageing muscles, in vitro primary cells derived from vastus lateralis of young and aged subjects were cultured. Both initiator caspases and effector caspases in the presence or absence of specific or broad pharmacologic inhibitors were analysed. Furthermore, the expression of various genes that play a critical role in oxidative stress and cell death was evaluated. The findings highlighted an increased rate of spontaneous apoptosis and an up-regulation of CASP2, 6, 7, 9 and other cell death genes in aged SCs, supporting the hypothesis of an intrinsic ageing of SCs and previous reports demonstrating an increased susceptibility to apoptosis of SCs from old animals. These results suggest that a greater proportion of SCs from old subjects might undergo programmed cell death in vivo in response to stressful stimuli, thereby impairing skeletal muscle regeneration.