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Paper Information

Title: 

MYOSTATIN AND IGF-1 PATHWAYS IN RELATION WITH APOPTOSIS IN EXPERIMENTAL NON ISCHEMIC DILATED CARDIOMYOPATHY

Type: POSTER
Author(s): MAHMOUDABADI M.,RAY L.,MATHIEU M.,DEWACHTER C.,HADAD I.,JESPERS P.,NAEIJE R.,MC ENTEE K.
 
 
 
Name of Seminar: IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY
Type of Seminar:  CONGRESS
Sponsor:  PHYSIOLOGY AND PHARMACOLOGY SOCIETY, MASHHAD UNIVERSITY OF MEDICAL SCIENCE
Date:  2007Volume 18
 
 
Abstract: 

Introduction: Myostatin (MSTN), a transforming growth factor-β family member, is an essential negative regulator of muscle growth. Its intracellular signalling is transmitted by activin type I (ActRI) and II receptors (ActRIIA and ActRIIB). Myostatin is also expressed in the myocardium and could play an important role in remodelling associated with cardiac diseases. It is considered as a proapoptotic, Akt-inactivating factor. On the other hand, IGF-1, modulates cardiac mass by preventing apoptosis through its receptor (IGFR1) and activation of Akt. Myostatin is the cardiac chalone of IGF-1.
Objective: We studied the time course of myocardial expression of MSTN and IGF-1 systems together with biochemical markers of apoptosis in a model of dilated cardiomyopathy.
Methods: Relative expression of target genes was measured by RTQ-PCR on weekly repeated endomyocardial biopsies taken from 15 dogs during development (7 weeks) of rapid pacing induced heart failure.
Results: Gene expression of IGF-1, MSTN and ActRI remained unchanged. IGF1R progressively decreased from week 3. ActRIIa was mildly decreased from week 3 while ActRIIb decreased early and progressively; the downregulation of ActRIIb was already significant at week 1 and its level of expression at week 7 was half the basal level. Gene expression of the apoptotic effector caspase 3 early and progressively increased from week 1; a maximal 2.4 fold upregulation was observed at week 5 of the pacing period. However the apoptotic index Bcl-2/Bax stayed unchanged during the course of the disease.
Conclusion: These results suggest that an imbalance of MSTN and IGF-1 signalling plays a minor role in the remodeling associated with tachycardiomyopathy.

 
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