Human bone marrow stem cells co-cultured with neonatal rat cardiomyocytes display limited cardiomyogenic plasticity

Bone Marrow-Derived Human Mesenchymal Stem Cells Express Cardiomyogenic Proteins But Do Not Exhibit Functional Cardiomyogenic Differentiation Potential

“…Recent studies on hBM-MSCs reported on cardiomyogenic differentiation in vitro [39][40][41][42]. However, hBM-MSCs co-cultured with neonatal rat cardiomyocytes displayed limited cardiomyogenic plasticity [43], and treatment with 5-azacytidine caused despite the absence of differentiation of hMSCs into cardiomyocytes, profound changes in current density [44]. Finally, a recent study could not provide evidence of functional cardiomyogenic differentiation of murine BM-MSCs [16].…”

Bone marrow-derived mesenchymal stem cells promote colorectal cancer progression through paracrine neuregulin 1/HER3 signalling

“…Human BM-MSC were isolated from sternal bone marrow aspirates, as previously described 21. Human T-MC and normal tissue-associated mesenchymal cells (N-MC) were isolated from colorectal adenocarcinoma resection specimens from three patients (more details in supplementary materials and methods and supplementary figure 1, available online only).…”

Mesenchymal Stem Cells for Cardiac Therapy: Practical Challenges and Potential Mechanisms

“…While the capacity of MSCs to form the cardiac lineage has been well documented, Koninckx and colleagues argue that the markers of cardiac differentiation in bone marrow transdifferentiated cells fail to show a mature phenotype, suggesting that terminal differentiation is incomplete [10]. A similar observation was made by Acquistapace and colleagues with MSCs when nanotube formation was inhibited, suggesting that transdifferentiation in particular, and not reprogramming to a progenitor state, is incomplete [22].…”

“…In addition to regenerating bone, fat and cartilage, recent transplant studies have reported that MSCs can also localize to the site of cardiac injury or ischemia [4, 5] and improve cardiac function [6–9], suggesting that MSCs retain an extensive plasticity governed by their environment. In vitro work (Table 1) has shown that coculture of human MSCs and rat neonatal cardiomyocytes (CMs) leads to MSC expression of two markers of cardiac lineage, troponin T and GATA4, although no sarcomeric organization has been observed [10]. Not only does this finding suggest that the cardiac microenvironment enhances the maturation of MSC-derived cardiomyocytes [10] but the formation of a cardiac progenitor-like cell from an MSC suggests that MSC transplantation may be a viable clinical treatment for repopulating damaged myocardium.…”

“…In vitro work (Table 1) has shown that coculture of human MSCs and rat neonatal cardiomyocytes (CMs) leads to MSC expression of two markers of cardiac lineage, troponin T and GATA4, although no sarcomeric organization has been observed [10]. Not only does this finding suggest that the cardiac microenvironment enhances the maturation of MSC-derived cardiomyocytes [10] but the formation of a cardiac progenitor-like cell from an MSC suggests that MSC transplantation may be a viable clinical treatment for repopulating damaged myocardium. However, given that early studies used bone marrow derived mononuclear cells (BMMNCs) that contained a mixed cell population, the ability of MSCs to improve cardiac function in vivo (Table 2) remains controversial since it is uncertain whether the beneficial effect of these earlier studies was actually due to the MSCs within the unpurified population or possibly due to another cell type.…”