Fibroblasts are critical in supporting normal wound healing. In fact, they are involved in key processes of wound regeneration, as fibrin clot, the creation of new extracellular matrix (ECM) and collagen structures to support the other cells associated with effective wound healing, as well as contracting the wound [1]. Autologous micrograft (AMG) therapies have recently emerged as a new effective treatment able to improve wound healing capacity [2]. This innovative technique, based on autologous micrografts, called Rigenera®, is able to restore several tissue damage using a promising CE-certified medical device called Rigeneracons. Its efficacy was demonstrated in the wound care including the management of chronic or non-healing wounds (ulcers, dehiscences, pathological scars) and for hard tissues and cartilage regeneration [3]. However, the molecular mechanisms connecting their beneficial outcomes with the wound healing process are still unrevealed. Here, we show that AMG modulates primary fibroblast migration and accelerates skin re-epithelialization without affecting cell proliferation. We demonstrate that AMG is enriched in a pool of growth factors that may provide the initiation signal for faster endogenous wound healing response. This, in turn, leads to increased cell migration rate by elevating activity of extracellular signals-regulated kinase (ERK) and subsequent activation of matrix metalloproteinase expression and their extracellular enzymatic activity. Overall, we showed the molecular mechanisms through which AMG supports and triggers wound healing process

The investigation of the effects of autologous micrografts in the process of wound healing / Ronzoni, F; Balli, M; Benedetti, L; Graziano, A; Sampaolesi, M; Cusella De Angelis, M. G; Ceccarelli, G.. - (2019). (Intervento presentato al convegno 73° Congresso Società Italiana di Anatomia e Istologia tenutosi a Napoli).

The investigation of the effects of autologous micrografts in the process of wound healing

Sampaolesi, M;
2019

Abstract

Fibroblasts are critical in supporting normal wound healing. In fact, they are involved in key processes of wound regeneration, as fibrin clot, the creation of new extracellular matrix (ECM) and collagen structures to support the other cells associated with effective wound healing, as well as contracting the wound [1]. Autologous micrograft (AMG) therapies have recently emerged as a new effective treatment able to improve wound healing capacity [2]. This innovative technique, based on autologous micrografts, called Rigenera®, is able to restore several tissue damage using a promising CE-certified medical device called Rigeneracons. Its efficacy was demonstrated in the wound care including the management of chronic or non-healing wounds (ulcers, dehiscences, pathological scars) and for hard tissues and cartilage regeneration [3]. However, the molecular mechanisms connecting their beneficial outcomes with the wound healing process are still unrevealed. Here, we show that AMG modulates primary fibroblast migration and accelerates skin re-epithelialization without affecting cell proliferation. We demonstrate that AMG is enriched in a pool of growth factors that may provide the initiation signal for faster endogenous wound healing response. This, in turn, leads to increased cell migration rate by elevating activity of extracellular signals-regulated kinase (ERK) and subsequent activation of matrix metalloproteinase expression and their extracellular enzymatic activity. Overall, we showed the molecular mechanisms through which AMG supports and triggers wound healing process
2019
73° Congresso Società Italiana di Anatomia e Istologia
04 Pubblicazione in atti di convegno::04b Atto di convegno in volume
The investigation of the effects of autologous micrografts in the process of wound healing / Ronzoni, F; Balli, M; Benedetti, L; Graziano, A; Sampaolesi, M; Cusella De Angelis, M. G; Ceccarelli, G.. - (2019). (Intervento presentato al convegno 73° Congresso Società Italiana di Anatomia e Istologia tenutosi a Napoli).
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1581825
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