Recent evidence suggests that ageing-related diseases could result in an accelerated loss of self-renewal capability of adult stem cells, normally involved in replacing damaged cellular elements. In previous works, we highlighted that a specific treatment, named tissue optimization-regenerative (TO-RGN), of radio-electric asymmetric conveyer (REAC) technology, influenced gene expression profiles controlling stem cell differentiation and pluripotency of human skin-derived fibroblastsin vitro. The purpose of the present work was to verify whether TO-RGN may also be effective in counteracting the expression of the senescence marker beta-galactosidase and of senescence-associated gene expression patterning, engaged during prolonged culture of human adipose-derived stem cells (hADSCs). Following TO-RGN exposure, we observed a significant downregulation in beta-galactosidase staining and in the expression of the senescence mediator genes p16INK4, ARF, p53, and p21CIP1. Moreover, differently formed untreated cells, TO-RGN-exposed hADSCs maintained their typical fibroblast-like morphology and exhibited a multilineage potential even at late passages, as shown by the remarkable preservation of commitment to osteogenic, adipogenic, chondrogenic, and vasculogenic fates, both at morphologic and gene expression levels. In conclusion, our study highlights a positive effect of TO-RGN in counteracting degenerative senescence processesin vitro.

Anti-senescence efficacy of radio-electric asymmetric conveyer technology / Maioli, Margherita; Rinaldi, S; Santaniello, S; Castagna, A; Pigliaru, G; Delitala, A; Lotti Margotti, M; Bagella, Luigi Marco; Fontani, V; Ventura, C.. - In: AGE. - ISSN 2452-0756. - 36:1(2014), pp. 9-20. [10.1007/s11357-013-9537-8]

Anti-senescence efficacy of radio-electric asymmetric conveyer technology

MAIOLI, Margherita;Delitala A;BAGELLA, Luigi Marco;
2014-01-01

Abstract

Recent evidence suggests that ageing-related diseases could result in an accelerated loss of self-renewal capability of adult stem cells, normally involved in replacing damaged cellular elements. In previous works, we highlighted that a specific treatment, named tissue optimization-regenerative (TO-RGN), of radio-electric asymmetric conveyer (REAC) technology, influenced gene expression profiles controlling stem cell differentiation and pluripotency of human skin-derived fibroblastsin vitro. The purpose of the present work was to verify whether TO-RGN may also be effective in counteracting the expression of the senescence marker beta-galactosidase and of senescence-associated gene expression patterning, engaged during prolonged culture of human adipose-derived stem cells (hADSCs). Following TO-RGN exposure, we observed a significant downregulation in beta-galactosidase staining and in the expression of the senescence mediator genes p16INK4, ARF, p53, and p21CIP1. Moreover, differently formed untreated cells, TO-RGN-exposed hADSCs maintained their typical fibroblast-like morphology and exhibited a multilineage potential even at late passages, as shown by the remarkable preservation of commitment to osteogenic, adipogenic, chondrogenic, and vasculogenic fates, both at morphologic and gene expression levels. In conclusion, our study highlights a positive effect of TO-RGN in counteracting degenerative senescence processesin vitro.
2014
Anti-senescence efficacy of radio-electric asymmetric conveyer technology / Maioli, Margherita; Rinaldi, S; Santaniello, S; Castagna, A; Pigliaru, G; Delitala, A; Lotti Margotti, M; Bagella, Luigi Marco; Fontani, V; Ventura, C.. - In: AGE. - ISSN 2452-0756. - 36:1(2014), pp. 9-20. [10.1007/s11357-013-9537-8]
File in questo prodotto:
File Dimensione Formato  
2013Maioli et al Age Anti senescence efficacy.pdf

accesso aperto

Tipologia: Versione editoriale (versione finale pubblicata)
Licenza: DRM non definito
Dimensione 807.95 kB
Formato Adobe PDF
807.95 kB Adobe PDF Visualizza/Apri

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11388/62965
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 32
  • ???jsp.display-item.citation.isi??? 31
social impact