Papers by Keyword: Cardiomyocyte

Abstract: We previously reported that P19.CL6 cells can be cultured in porous hydroxyapatite ceramics prepared by firing green compacts consisting of apatite fibers and spherical carbon beads (150 μm in diameter). Cells cultured for 20 days in an apatite-fiber scaffold (AFS) proliferated and differentiated into cells expressing troponin T, a cardiomyocyte-specific gene, but the expression level was insufficient to support the functional maturation of cells required for biomedical device applications. In this study, we aimed to optimize the internal AFS environment for cardiomyocytes by mixing two sizes (150-and 20-μm) of carbon beads. P19.CL6 cells were cultured in AFS materials comprising different carbon ratios in the presence of alpha-MEM with (AFS+) or without (AFS-) dimethyl sulfoxide (DMSO), and cell growth and gene expression were assessed. We found that AFS(50, 1:1 ratio) is the most suitable scaffold for the proliferation and differentiation of P19.CL6 cells and the addition of DMSO to the culture medium is necessary for differentiation into cardiomyocytes. We also assessed the culture of P19.CL6 cells in AFS in a radial-flow bioreactor for several days.

Abstract: Organic electronic devices offer a convenient solution for bioelectronic sensor applications due to the biocompatibility of organic semiconductors and biologic tissues. So-called biosensors can convert electrochemical processes connected to cell membranes into electronic signals. A matrix of such biosensors can simultaneously scan a number of biological samples as well as living tissue in the body. The core of the device is a transistor, today mostly OECT (Organic Electro Chemical Transistor) fabricated by thin film or printing technique from semiconducting biocompatible polymer PEDOT:PSS (poly(3, 4-ethylenedioxythiophene) polystyrene sulfonate). Such transistors were printed both by inkjet and screen-printing technique and their main characteristics are presented.

Abstract: Heart development is a precisely harmonized process of cellular proliferation, migration, differentiation, and integrated morphogenetic interactions, and therefore it is extremely vulnerable to developmental defects that cause congenital heart diseases (CHD). One of the major causes of CHD has been shown to be the mutations in key cardiac channel-forming proteins namely, connexins (Cxs). Cxs are tetra-spanning transmembrane proteins that form gap junction channels and hemichannels on cellular membrane. They allow passage of small molecules or ions between adjacent cells or between cells and the extracellular environment. Studies have revealed that the spatiotemporal expression of Cxs mainly, Cx31.9, Cx40, Cx43, and Cx45 is essentially involved in early developmental events, morphogenetic transformations, maturation, and functional significance of heart. Our lab and others have shown that mutations in gap junction proteins could result in impaired trafficking, misfolding, and improper channel function of these proteins. It has also been shown that differential expressions of cardiac Cxs are associated with pathophysiological conditions of heart. Collectively, these conditions are coupled with abrogated or modified functionality of relevant channels in cardiac tissue, which are associated with many pathological situations, including CHD. Since CHD are a major cause of morbidity, therefore recovery of such kind of heart defects associated with Cxs is extremely important but remains highly challenging. In this review, we will summarize the role of Cxs in development, morphogenesis, maturation, normal function, and pathology of heart, and propose possible bioengineering techniques to recover defects in cardiac tissues related to the modified functions of Cxs.

Abstract: To obtain an enhanced population of cardiomyocytes from differentiating mouse embryonic stem (ES) cells, we confirmed the role of noggin treatment during the cardiac differentiation of mouse ES cells. ES cells were cultured in ES medium containing both noggin and LIF for 3 days on the mouse embryonic fibroblast feeder layer, followed by dissociated and suspension culture without LIF to form the embryoid body (EB). The next day, noggin was eliminated and EBs were cultured continuously. Noggin treated ES cells showed a relatively rapid increase of cardiac marker genes, while the vehicle (PBS) treated group showed no significant cardiac marker expression at 4 days after the EB formation. Furthermore, Noggin treated ES cells showed 68.00±9.16% spontaneous beating EBs at 12 days after the EB formation. To develop a more efficient cardiomyocyte differentiation method, we tested several known cardiogenic reagents (ascorbic acid, 5’-Azacytidine, LiCl, oxytocin, FGF2 and PDGF-BB) after noggin induction or we cultured noggin treated ES cells on various extracellular matrixes (collagen, fibronectin and Matrigel). Quantitative RT-PCR and immunocytochemistry results showed a significantly increased cardiac differentiation rate in the FGF2 treated group. Differentiation on the collagen extracellular matrix (ECM) could slightly increase the cardiac differentiation efficiency. These results show the possibilities for the establishment of selective differentiation conditions for the cardiac differentiation of mouse ES cells.