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MicroRNA-23a is involved in tumor necrosis factor-α induced apoptosis in mesenchymal stem cells and myocardial infarction
- Source :
- Experimental and Molecular Pathology. 97:23-30
- Publication Year :
- 2014
- Publisher :
- Elsevier BV, 2014.
-
Abstract
- Cell therapy has emerged as an attractive therapeutic modality to treat myocardial infarction (MI) via repairing damaged myocardium, and mesenchymal stem cells (MSCs) are an appealing therapeutic approach for cardiac regeneration. However, the clinical application of MSC-based therapy is restricted because of the poor survival of implanted cells, and this poor survival remains poorly understood. Using a tumor necrosis factor (TNF)-α-induced bone marrow (BM)-MSC injury model in vitro and a rat MI model in vivo, we showed in the current study that miR-23a was involved in TNF-α-induced BM-MSC apoptosis through regulating caspase-7 and that the injection of BM-MSCs overexpressing miR-23a could improve left ventricular (LV) function and reduce infarct size in the rat MI model. Our findings elucidate the etiology of MI and provide an alternative treatment strategy for patients with heart failure caused by MI who are not optimal candidates for surgical treatment.
- Subjects :
- Male
Pathology
medicine.medical_specialty
Heart Ventricles
Clinical Biochemistry
Myocardial Infarction
Apoptosis
Mesenchymal Stem Cell Transplantation
Pathology and Forensic Medicine
Rats, Sprague-Dawley
Cell therapy
In vivo
medicine
Animals
Humans
Myocardial infarction
3' Untranslated Regions
Molecular Biology
Cells, Cultured
Caspase 7
Dose-Response Relationship, Drug
Tumor Necrosis Factor-alpha
business.industry
Mesenchymal stem cell
Mesenchymal Stem Cells
medicine.disease
Rats
Disease Models, Animal
MicroRNAs
HEK293 Cells
medicine.anatomical_structure
Gene Expression Regulation
Heart failure
Tumor necrosis factor alpha
Bone marrow
business
Subjects
Details
- ISSN :
- 00144800
- Volume :
- 97
- Database :
- OpenAIRE
- Journal :
- Experimental and Molecular Pathology
- Accession number :
- edsair.doi.dedup.....f5581a8585828908b59268b245ecdfe0