Met-Activating Genetically Improved Chimeric Factor-1 (Magic-F1) is a human recombinant protein derived from hepatocyte growth factor/scatter factor (HGF/SF) and consists in two Met-binding domains repeated in tandem and separated by an artificial linker. It has a reduced affinity for Met and, in contrast to HGF, it elicits activation of the AKT but not the ERK signaling pathway. We recently showed that Magic-F1 induces muscle cell hypertrophy but not progenitor cell proliferation, both in vitro and in vivo where a transgenic mouse express the recombinant protein exclusively in skeletal muscle tissue [1]. Here, we examined the temporal and spatial expression pattern of Magic-F1 in comparison with Pax3 (paired box gene 3) transcription factor during embryogenesis [2]. Ranging from 9.5 to 17.5 dpc (days post coitum) mouse embryos were analyzed by in situ hybridization using whole mounts during early stages of development (9.5-10.5-11.5 dpc) and cryostat sections for later stages (11.5-13.5-15.5-17.5 dpc). We found that Magic-F1 is expressed in developing organs and tissues of mesenchymal origin, where Pax3 signal appears to be downregulated respect to the wt embryos. These data suggest that Magic-F1 could be responsible of muscular hypertrophy, cooperating with Pax3 signal pathway in skeletal muscle precursor cells

Magic-F1 transgene cooperates with Pax 3 during early myogenesis to induce muscular hypertrophy / Ronzoni, FLAVIO LORENZO; Ceccarelli, Gabriele; Biressi, S; Galli, Daniela; Cassano, M; Benedetti, Laura; Vercesi, Luigi; CUSELLA DE ANGELIS, MARIA GABRIELLA; Sampaolesi, Maurilio. - (2012). (Intervento presentato al convegno 66th Meeting of Italian Society of Anatomy and Histology tenutosi a Pistoia).

Magic-F1 transgene cooperates with Pax 3 during early myogenesis to induce muscular hypertrophy

SAMPAOLESI, MAURILIO
2012

Abstract

Met-Activating Genetically Improved Chimeric Factor-1 (Magic-F1) is a human recombinant protein derived from hepatocyte growth factor/scatter factor (HGF/SF) and consists in two Met-binding domains repeated in tandem and separated by an artificial linker. It has a reduced affinity for Met and, in contrast to HGF, it elicits activation of the AKT but not the ERK signaling pathway. We recently showed that Magic-F1 induces muscle cell hypertrophy but not progenitor cell proliferation, both in vitro and in vivo where a transgenic mouse express the recombinant protein exclusively in skeletal muscle tissue [1]. Here, we examined the temporal and spatial expression pattern of Magic-F1 in comparison with Pax3 (paired box gene 3) transcription factor during embryogenesis [2]. Ranging from 9.5 to 17.5 dpc (days post coitum) mouse embryos were analyzed by in situ hybridization using whole mounts during early stages of development (9.5-10.5-11.5 dpc) and cryostat sections for later stages (11.5-13.5-15.5-17.5 dpc). We found that Magic-F1 is expressed in developing organs and tissues of mesenchymal origin, where Pax3 signal appears to be downregulated respect to the wt embryos. These data suggest that Magic-F1 could be responsible of muscular hypertrophy, cooperating with Pax3 signal pathway in skeletal muscle precursor cells
2012
66th Meeting of Italian Society of Anatomy and Histology
04 Pubblicazione in atti di convegno::04b Atto di convegno in volume
Magic-F1 transgene cooperates with Pax 3 during early myogenesis to induce muscular hypertrophy / Ronzoni, FLAVIO LORENZO; Ceccarelli, Gabriele; Biressi, S; Galli, Daniela; Cassano, M; Benedetti, Laura; Vercesi, Luigi; CUSELLA DE ANGELIS, MARIA GABRIELLA; Sampaolesi, Maurilio. - (2012). (Intervento presentato al convegno 66th Meeting of Italian Society of Anatomy and Histology tenutosi a Pistoia).
File allegati a questo prodotto
Non ci sono file associati a questo prodotto.

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/11573/1581985
 Attenzione

Attenzione! I dati visualizzati non sono stati sottoposti a validazione da parte dell'ateneo

Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus ND
  • ???jsp.display-item.citation.isi??? ND
social impact