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Metabolic pathways are altered in skeletal muscle satellite cells (SC) in heart failure (HF)

Session Moderated Poster Session 5 - Basic mechanisms in heart failure

Speaker Victoria Galenko

Event : Heart Failure 2015

  • Topic : arrhythmias and device therapy
  • Sub-topic : Cellular Electrophysiology
  • Session type : Moderated Posters

Authors : VL Galenko (St Petersburg,RU), P Tikanova (St Petersburg,RU), MA Bortsova (St Petersburg,RU), TA Lelyavina (St Petersburg,RU), MYU Sitnikova (St Petersburg,RU), R Dmitrieva (St Petersburg,RU)

VL Galenko1 , P Tikanova2 , MA Bortsova1 , TA Lelyavina1 , MYU Sitnikova1 , R Dmitrieva2 , 1 Federal Almazov Medical Research Centre, Research Department for Heart Failure - St Petersburg - Russian Federation , 2 Federal Almazov Medical Research Centre, Institute of Molecular Biology and Genetics - St Petersburg - Russian Federation ,

European Journal of Heart Failure Abstracts Supplement ( 2015 ) 17 ( Supplement 1 ), 253

Background and Aim: Chronic activation of natriuretic peptides (NP) system in combination with mitochondrial disfunction and/or defects in fatty acids (FA) oxidation are proposed as the possible mechanisms of the progression of systemic metabolic disorders in cardiovascular patients. Systemic metabolic derangements in HF were demonstrated for many tissues; however, how these alterations affect SC remains largely unknown. Our work was aimed to study the functional alterations in SC from HF patients using cellular in vitro models.

Methods: soleus muscle samples were obtained from 3 healthy donors (HD) and 7 HF patients (NYHA III; age 49+11; LVEF 31+5%); SCs were purified from muscle tissue, and myogenesis of SC was stimulated in vitro to confirm differentiation potential. Immunostaining for MHC was performed co confirm differentiation. Dynamics of gene expression for myogenic markers (Pax7, Pax3, MyoG, Myf5, Mrf4, Six4) and metabolic regulators (PPARg, aP2, Pgc1a, NP system genes) during differentiation was determined by Q-PCR.

Results: The most important observations are demonstrated on figure. We have found that genes involved in FA utilization (aP2), and insulin-sensitive glucose transporter (GLUT4) were downregulated in SC from HF patients. We have found that genes involved in FA utilization (aP2), and insulin-sensitive glucose transporter (GLUT4) were downregulated in SC from HF patients. Moreover, the downregulation of NPs system at mRNA level was demonstrated for HF-derived SC, while expression of PPARg and Pgc1a was increased. Finally, the dynamics of markers of myogenesis was altered in HF SC.

Conclusion: The systemic metabolic derangements in HF affect SC functions that may result in muscular disorders including failure of regeneration, muscle wasting and cachexia.

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