ER71 directs mesodermal fate decisions during embryogenesis.

Er71 mutant embryos are nonviable and lack hematopoietic and endothelial lineages. To further define the functional role for ER71 in cell lineage decisions, we generated genetically modified mouse models. We engineered an Er71-EYFP transgenic mouse model by fusing the 3.

Molecular cardiology in translation: gene, cell and chemical-based experimental therapeutics for the failing heart.

Acquired and inherited diseases of the heart represent a major health care issue in this country and throughout the World. Clinical medicine has made important advancements in the past quarter century to enable several effective treatment regimes for cardiac patients. Nevertheless, it is apparent that even with the best care, current treatment strategies and therapeutics are inadequate for treating heart disease, leaving it arguably the most pressing health issue today.

Partial induction of the myogenic program in noncommitted adult stem cells.

The ability of multipotent adult stem cells (MASCs) and mesenchymal stem cells (MSCs) to acquire certain biochemical and functional properties of differentiated cells in response to various inductive cues has raised hopes to utilize such cells for therapeutic purposes. It is of particular importance to define precisely the differentiation status of induced MASCs and MSCs, and to determine the signaling pathways that control their differentiation. The identification of such signals might help to expand and enhance specific differentiation pathways to allow the formation of fully functional muscle cells from undetermined stem cells.

Efficient homing of multipotent adult mesenchymal stem cells depends on FROUNT-mediated clustering of CCR2.

Circulating stem cells of different origin have been demonstrated to improve repair of various organs both after systemic and local application, although the mechanisms that cause these effects are still not fully understood. We have used a combination of DNA microarray analysis and in vitro migration assays to screen for molecules that mediate homing of long-term renewing adult bone marrow-derived multipotent mesenchymal stem cells (BM-MASCs). We show that the cytokine receptor CCR2 is necessary for organ-specific homing of bone marrow-derived MASCs to the heart in a transgenic mouse model and into hearts damaged by ischemia/reperfusion.

Differentiation versus plasticity: fixing the fate of undetermined adult stem cells.

Adult mesenchymal stem cells own a considerable plasticity, which enables them to respond to various extra- and intracellular cues and exert, at least partially, various differentiation pathways. Recently, we have shown that multipotent adult stem cells (MASCs) derived from the mouse bone marrow (mBM-MASCs) consist of distinct cell populations that have similar differentiation abilities but differ in the expression of several stem cell markers. Despite their remarkable developmental potential MASCs seem to miss crucial components to complete specific differentiation programs necessary to acquire a fully functional phenotype.

Activation of myogenic differentiation pathways in adult bone marrow-derived stem cells.

During embryogenesis, various cell types can be programmed by potent inducers to follow distinct differentiation paths. In adult life, this ability seems to be restricted to specific multipotent cells. We have identified two cell populations from adult murine bone marrow which express various "stemness" genes.

Mesenchymal stem cells are recruited to striated muscle by NFAT/IL-4-mediated cell fusion.

Mesenchymal stem cells (MSCs) or mesenchymal adult stem cells (MASCs) that are present in the stroma of several organs have been proposed to contribute to the regeneration of different tissues including liver, blood, heart, and skeletal muscle. Yet, it remains unclear whether MSCs can be programmed to differentiate cell-autonomously into fully functional cells or whether they are recruited by surrounding cells via fusion and thereby acquire specialized cellular functions. Here, we demonstrate that Wnt signaling molecules activate the expression of distinct sets of genes characteristic for cardiac and skeletal muscle cells in MASCs.