title: Primary skeletal muscle myoblasts from chronic heart failure patients exhibit loss of anti-inflammatory and proliferative activity.
abstract: Peripheral skeletal muscle wasting is a common finding with adverse effects in chronic heart failure (HF). Whereas its clinical relevance is beyond doubt, the underlying pathophysiological mechanisms are not yet fully elucidated. We aimed to introduce and characterize the primary culture of skeletal muscle cells from individual HF patients as a supportive model to study this muscle loss.
  
  
  
  Primary myoblast and myotubes cultures were successfully propagated from the m. vastus lateralis of 6 HF patients with reduced ejection fraction (HFrEF; LVEF <45 %) and 6 age and gender-matched healthy donors. HFrEF cultures were not different from healthy donors in terms of morphology, such as myoblast size, shape and actin microfilament. Differentiation and fusion indexes were identical between groups. Myoblast proliferation in logarithmic growth phase, however, was attenuated in the HFrEF group (p = 0.032). In addition, HFrEF myoblasts are characterized by a reduced TNFR2 expression and IL-6 secretion (p = 0.017 and p = 0.016; respectively).
  
  
  
  Biopsy derived primary skeletal muscle myoblasts of HFrEF patients produce similar morphological and myogenic differentiation responses as myoblasts of healthy donors, though demonstrate loss of anti-inflammatory and proliferative activity.
authors.affiliation: Laboratory of Cellular and Molecular Cardiology, Antwerp University Hospital, Edegem, Belgium. tahnee.sente@uantwerpen.be.|Department of Translational Pathophysiological Research, Cardiovascular Diseases, University of Antwerp, Wilrijk, Belgium. tahnee.sente@uantwerpen.be.
authors.forename: Tahnee
authors.initials: T
authors.lastname: Sente
authors.affiliation: Department of Cardiology, Antwerp University Hospital, Edegem, Belgium.
authors.forename: An M
authors.initials: AM
authors.lastname: Van Berendoncks
authors.affiliation: Department of Pediatric Neurology, UZ Brussel, Vrije Universiteit Brussel (VUB), Brussels, Belgium.
authors.forename: An I
authors.initials: AI
authors.lastname: Jonckheere
authors.affiliation: Department of Pediatrics, Nijmegen Center for Mitochondrial Disorders, Translational Metabolic Laboratory, Radboud University Medical Center, Nijmegen, The Netherlands.
authors.forename: Richard J
authors.initials: RJ
authors.lastname: Rodenburg
authors.affiliation: Department of Thoracic and Vascular Surgery, Antwerp University Hospital, Edegem, Belgium.
authors.forename: Patrick
authors.initials: P
authors.lastname: Lauwers
authors.affiliation: Department of Biochemistry, Antwerp University Hospital, Edegem, Belgium.
authors.forename: Viviane
authors.initials: V
authors.lastname: Van Hoof
authors.affiliation: Center for Oncological Research (CORE) Antwerp, University of Antwerp, Wilrijk, Belgium.
authors.forename: An
authors.initials: A
authors.lastname: Wouters
authors.affiliation: Center for Oncological Research (CORE) Antwerp, University of Antwerp, Wilrijk, Belgium.
authors.forename: Filip
authors.initials: F
authors.lastname: Lardon
authors.affiliation: Laboratory of Cellular and Molecular Cardiology, Antwerp University Hospital, Edegem, Belgium.|Department of Cardiology, Antwerp University Hospital, Edegem, Belgium.
authors.forename: Vicky Y
authors.initials: VY
authors.lastname: Hoymans
authors.affiliation: Laboratory of Cellular and Molecular Cardiology, Antwerp University Hospital, Edegem, Belgium.|Department of Translational Pathophysiological Research, Cardiovascular Diseases, University of Antwerp, Wilrijk, Belgium.|Department of Cardiology, Antwerp University Hospital, Edegem, Belgium.
authors.forename: Christiaan J
authors.initials: CJ
authors.lastname: Vrints
mesh_terms: D016022:Case-Control Studies; D049109:Cell Proliferation; D002478:Cells, Cultured; D016922:Cellular Senescence; D002908:Chronic Disease; D005260:Female; D006333:Heart Failure / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D015850:Interleukin-6 / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009133:Muscular Atrophy / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D032448:Myoblasts, Skeletal / Q000378:metabolism / Q000473:pathology*; D018006:Myogenic Regulatory Factors / Q000378:metabolism; D000072041:PAX3 Transcription Factor / Q000378:metabolism; D051763:PAX7 Transcription Factor / Q000378:metabolism; D010641:Phenotype; D061251:Primary Cell Culture; D052097:Quadriceps Muscle / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D047889:Receptors, Tumor Necrosis Factor, Type II / Q000378:metabolism; D015398:Signal Transduction; D013318:Stroke Volume; D013997:Time Factors; D016277:Ventricular Function, Left
chemical_list: C508600:IL6 protein, human; D015850:Interleukin-6; D018006:Myogenic Regulatory Factors; D000072041:PAX3 Transcription Factor; C489409:PAX3 protein, human; D051763:PAX7 Transcription Factor; C497321:PAX7 protein, human; D047889:Receptors, Tumor Necrosis Factor, Type II; C415902:TNFRSF1B protein, human
keywords: Chronic heart failure; Muscle wasting; Myoblast cultures; xCELLigence