Abstract
Under myocardial microenvironment, bone marrow-derived mesenchymal stem cells (MSCs) can transdifferentiate into cardiomyocytes (CMs). However, the role of histone deacetylase 1 (HDAC1) in this directed differentiation process remains unclear. The current study is to determine the acetylation regulatory mechanisms that may be involved in the directed CM differentiation from MSCs. MSCs isolated from male Sprague-Dawley (SD) rats were marked with Ad-EGFP and co-cultured with CMs. Flow cytometry was used to sort EGFP-positive (EGFP+) MSCs from the co-culture system. Then, the expression of cardiac troponin T (cTnT) in these MSCs was detected by immunofluorescence assay. In addition, HDAC1 levels at different co-culture times were measured by quantitative real-time polymerase chain reaction (QT-PCR) and Western blotting. At 4 days after co-culture with CMs, the MSCs began to expression detectable levels of cTnT. The expression of HDAC1 in CMs was much lower than that in MSCs. After co-culture with CMs, the expression of HDAC1 in MSCs was significantly decreased in a time dependent manner. In addition, our recent study has also identified that knockdown of the HDAC1 could promote the directed differentiation of MSCs into CMs. The results suggest that HDAC1 has a negative correlation with cardiac cell differentiation from MSCs under a myocardial microenvironment. HDAC1 might play an important role in the directed differentiation of MSCs into CMs in heart.
Highlights
Bone marrow-derived mesenchymal stem cells (MSCs) exhibit strong capabilities of self-renewal and tri-lineage differentiation and are suitable for autologous stem cell therapy in many diseases including ischemic heart disease
This study demonstrated that MSCs could differentiate into CM phenotypes in a myocardial microenvironment
When the MSCs co-cultured with CMs, the expression of histone deacetylase 1 (HDAC1) was significantly decreased in a time-dependent manner
Summary
Bone marrow-derived mesenchymal stem cells (MSCs) exhibit strong capabilities of self-renewal and tri-lineage differentiation and are suitable for autologous stem cell therapy in many diseases including ischemic heart disease. MSCs are able to differentiate into tissue-specific mature cells in their targeted organs, in which the tissue-specific microenvironment plays important roles. Recent studies have revealed that epigenetic changes in DNA methylation and chromatin structure critical in the determination of lineage-specific differentiation of MSCs [2]. In this respect, histone deacetylase inhibitors have been reported to have strong effects on MSC differentiation [3]. The epigenetic modification of histone acetylation has been identified to play an important role in the transdifferentiation processes of adult stem cells
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