Arginine-Vasopressin (AVP) is a neurohypophyseal hormone able to induce differentiation in myogenic cell lines and primary satellite cells. V1aR is the only AVP receptor expressed in skeletal muscle. By interacting with V1aR, AVP activates phospholipases C and D, increases cytosolic Ca2+ concentrations and regulates cAMP levels. The AVP-dependent increase in cytosolic calcium activates CaMK and calcineurin pathways resulting in the formation of multifactor complexes on the promoter of muscle specific genes. Our previous data demonstrate that V1aR expression is modulated during muscle regeneration and the stimulation of AVP signaling strongly enhances regeneration of injured muscles. In an experimental model of muscular atrophy induced by TNF over-expression, stimulation of AVP pathways counteracts the negative effects of TNF both enhancing regeneration and inhibiting inflammation. The molecular analysis for the expression levels of early and late regeneration markers (Pax7 and MyoD or myogenin and MHC, respectively) suggested an impairment of regeneration in muscles over-expressing TNF. This effect was counteracted by V1aR overexpression. The positive effects of V1aR on muscle homeostasis are due to the promotion of the calcinuerin-IL-4 pathway and by the inhibition of atrophic genes expression mediated by FOXO phosphorylation via Akt-dependant pathway. By all the above we are analyzing the effects of AVP signaling stimulation in mouse models of muscular dystrophies. Preliminary data demonstrate that stimulation of AVP-dependent pathways ameliorates inflammation and regeneration processes. This study highlights a novel in vivo role for the AVP-dependent pathways which may represent a potential gene therapy approach for many diseases affecting muscle homeostasis.

Exploiting Vasopressin signaling in muscular atrophy and dystrophies / Costa, Alessandra; Adamo, Sergio; Scicchitano, Bianca Maria. - (2012). (Intervento presentato al convegno IX meeting IIM tenutosi a Lecce, Italia nel 12-14 ottobre 2012).

Exploiting Vasopressin signaling in muscular atrophy and dystrophies

COSTA, ALESSANDRA;ADAMO, Sergio;SCICCHITANO, Bianca Maria
2012

Abstract

Arginine-Vasopressin (AVP) is a neurohypophyseal hormone able to induce differentiation in myogenic cell lines and primary satellite cells. V1aR is the only AVP receptor expressed in skeletal muscle. By interacting with V1aR, AVP activates phospholipases C and D, increases cytosolic Ca2+ concentrations and regulates cAMP levels. The AVP-dependent increase in cytosolic calcium activates CaMK and calcineurin pathways resulting in the formation of multifactor complexes on the promoter of muscle specific genes. Our previous data demonstrate that V1aR expression is modulated during muscle regeneration and the stimulation of AVP signaling strongly enhances regeneration of injured muscles. In an experimental model of muscular atrophy induced by TNF over-expression, stimulation of AVP pathways counteracts the negative effects of TNF both enhancing regeneration and inhibiting inflammation. The molecular analysis for the expression levels of early and late regeneration markers (Pax7 and MyoD or myogenin and MHC, respectively) suggested an impairment of regeneration in muscles over-expressing TNF. This effect was counteracted by V1aR overexpression. The positive effects of V1aR on muscle homeostasis are due to the promotion of the calcinuerin-IL-4 pathway and by the inhibition of atrophic genes expression mediated by FOXO phosphorylation via Akt-dependant pathway. By all the above we are analyzing the effects of AVP signaling stimulation in mouse models of muscular dystrophies. Preliminary data demonstrate that stimulation of AVP-dependent pathways ameliorates inflammation and regeneration processes. This study highlights a novel in vivo role for the AVP-dependent pathways which may represent a potential gene therapy approach for many diseases affecting muscle homeostasis.
2012
IX meeting IIM
04 Pubblicazione in atti di convegno::04d Abstract in atti di convegno
Exploiting Vasopressin signaling in muscular atrophy and dystrophies / Costa, Alessandra; Adamo, Sergio; Scicchitano, Bianca Maria. - (2012). (Intervento presentato al convegno IX meeting IIM tenutosi a Lecce, Italia nel 12-14 ottobre 2012).
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/510750
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