Skeletal Muscle Resident Progenitor Cells Coexpress Mesenchymal and Myogenic Markers and Are Not Affected by Chronic Heart Failure-Induced Dysregulations

Skeletal Muscle Resident Progenitor Cells Coexpress Mesenchymal and Myogenic Markers and Are Not Affected by Chronic Heart Failure-Induced Dysregulations

Background and Purpose. In heart failure (HF), metabolic alterations induce skeletal muscle wasting and decrease of exercise capacity and quality of life. The activation of skeletal muscle regeneration potential is a prospective strategy to reduce muscle wasting; therefore, the aim of this project w...

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Published in:Stem cells international Vol. 2019; no. 2019; pp. 1 - 11
Main Authors: Sergushichev, A., Sitnikova, M. Yu, Olga, Freylihman, Golovkin, A. S., Khromova, N. V., Tikanova, P. A., Ivanova, O. A., Galenko, V. L., Komarova, M. Y., Lelyavina, T. A., Dmitrieva, R., Bortsova, M. A.
Format: Journal Article
Language:English
Published: Cairo, Egypt Hindawi Publishing Corporation 01-01-2019
Hindawi
Hindawi Limited
Subjects:
Activation
Atrophy
Beta blockers
Biopsy
CD105 antigen
CD56 antigen
CD73 antigen
Cells (biology)
Chronic illnesses
Congestive heart failure
Diabetes
Environmental restoration
Exercise
Fitness training programs
Flow cytometry
Gastrocnemius muscle
Gene expression
Heart failure
Immunocytochemistry
Insulin resistance
Lipids
Markers
Mesenchyme
Metabolism
mRNA
Muscles
Musculoskeletal system
Myotubes
Oxidation
Patients
Physical fitness
Physiology
Progenitor cells
Properties (attributes)
Quality of life
Regeneration
Restoration
Skeletal muscle
Stem cells
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Summary:Background and Purpose. In heart failure (HF), metabolic alterations induce skeletal muscle wasting and decrease of exercise capacity and quality of life. The activation of skeletal muscle regeneration potential is a prospective strategy to reduce muscle wasting; therefore, the aim of this project was to determine if functional properties of skeletal muscle mesenchymal progenitor cells (SM-MPC) were affected by HF-induced functional and metabolic dysregulations. Methods. Gastrocnemius muscle biopsy samples were obtained from 3 healthy donors (HD) and 12 HF patients to purify mRNA for further analysis and to isolate SM-MPC. Cells were expanded in vitro and characterized by immunocytochemistry and flow cytometry for expression of mesenchymal (CD105/CD73/CD166/CD146/CD140b/CD140a/VIM) and myogenic (Myf5/CD56/MyoG) markers. Cells were induced to differentiate and were then analyzed by immunostaining and Q-PCR to verify the efficiency of differentiation. The expression of genes that control muscle metabolism and development was compared for HD/HF patients in both muscle biopsy and in vitro-differentiated myotubes. Results. The upregulation of MYH3/MYH8/Myf6 detected in HF skeletal muscle along with metabolic alterations indicates chronic pathological activation of the muscle developmental program. SM-MPC isolated from HD and HF patients represented a mixed population that coexpresses both mesenchymal and myogenic markers and differs from AD-MMSC, BM-MMSC, and IMF-MSC. The functional properties of SM-MPC did not differ between HD and HF patients. Conclusion. In the present work, we demonstrate that the metabolic and functional alterations we detected in skeletal muscle from HF patients do not dramatically affect the functional properties of purified and expanded in vitro SM-MPC. We speculate that skeletal muscle progenitor cells are protected by their niche and under beneficial circumstances could contribute to muscle restoration and prevention and treatment of muscle wasting. The potential new therapeutic strategies of HF-induced skeletal muscle wasting should be targeted on both activation of SM-MPC regeneration potential and improvement of skeletal muscle metabolic status to provide a favorable environment for SM-MPC-driven muscle restoration.
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Guest Editor: Zhaoping Ding
ISSN:1687-966X
1687-9678
DOI:10.1155/2019/5690345