Biomedical subjects

J M Felker

Publications and source records attributed to J M Felker.

3 recordsLinked to original sources

PubMed2001

Array analysis of the genes regulated during neuronal differentiation of human embryonal cells.

Recent advances in genetic technology have provided a new platform on which the simultaneous analysis of a large number of genes is possible in a rapid and efficient fashion. To assess the differential expression of human genes during neuronal differentiation, we compared the transcript profiles of undifferentiated, partially differentiated, and fully differentiated NT2/D1 cultures with cDNA expression arrays. Approximately 75 genes (13% of the gene array pool) were differentially expressed during neuronal development of NT2/D1 cells. Genes coding for pyruvate kinase M2 isozyme, clathrin assembly proteins, calmodulin, fibronectin, laminin, thymosin beta-10, and many others were upregulated as NT2/D1 cells differentiated into neurons. In contrast, several kinases, phosphatases, and G-protein coupled receptor genes showed downregulation upon neuronal differentiation. The information provided here is an invaluable reference for characterizing the phenotype of these cells. This information can also be used in cell therapy and transplantation in which the graft microenvironment and interaction with the host tissue is crucial.

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PubMed2000

The effects of bone morphogenetic protein 2 and 4 (BMP2 and BMP4) on gap junctions during neurodevelopment.

Nervous system deficits account for the third largest group of fatal birth defects (after heart and respiratory problems) in North America. Although considerable advance has been made in neuroscience research, the early events involved in neurogenesis remain to be elucidated. More specifically, the effects of signaling molecules on intercellular communication during neurodevelopment have not yet been studied. The development of the central nervous system is regulated, at least in part, by signaling molecules such as bone morphogenetic proteins (BMPs). In this study, we have used the embryonal mouse P19 cell line to examine the effects of BMP2 and BMP4 on gap junctional communication as well as neuronal and astrocytic differentiation. The undifferentiated P19 cells show high levels of the gap junction protein, connexin43 (Cx43), and functional intercellular coupling. However, Cx43 expression and dye coupling decrease as these cells differentiate into neurons and astrocytes. In contrast, cells treated with BMP2 or BMP4 lose their capacity to differentiate into neurons but not astrocytes, while they maintain extensive gap junctional communication. The very few neurons that remain in the BMP-treated cultures are coupled (a characteristic not seen in the control neurons). Together, our data suggest that BMPs may play a critical role in morphogenesis of P19 cells while they affect gap junctions.

Animals↗

PubMed1999

Human NT2/D1 cells differentiate into functional astrocytes.

As the most numerous cell type in the brain, astrocytes are coupled via gap junction channels. It is believed that communication among astrocytes is normally regulated by extracellular ions, neurotransmitters and neuromodulators. However, the level of astrocytic coupling is altered in abnormal conditions such as stroke, brain trauma and Alzheimer's disease. A well established human progenitor cell line, NT2/D1, has been previously differentiated into pure neuronal cultures. In the current study, for the first time, we report the differentiation of NT2/D1 cells into astrocytes, which express connexin43 and are coupled via gap junctions. Thus, human NT2/D1 cells are not merely committed neuronal progenitors but, similar to the embryonal stem cells, they can give rise to both lineages.

Astrocytes↗