Abstract: Embodiments of the present invention describe a method of changing the phenotype of monocytes and macrophages from a proinflammatory M1 phenotype to an anti-inflammatory M2 phenotype. The method can comprises providing a composition comprising a recombinant adeno-associated virus (rAAV) vector comprising an exogenous gene encoding ApoA-I Milano or a fragment thereof, and administering the composition to a mammal in need thereof to change the phenotype of monocytes or macrophages from a proinflammatory M1 phenotype to an anti-inflammatory M2 phenotype. By changing the phenotype of monocytes or macrophages from a proinflammatory M1 phenotype to an anti-inflammatory M2 phenotype, atherosclerosis can be treated. The present invention also describes a method of monitoring macrophage phenotypic switching and a method of assessing the efficacy of the treatment of atherosclerosis.

Abstract: Embodiments of the present invention describe a method of changing the phenotype of monocytes and macrophages from a proinflammatory M1 phenotype to an anti-inflammatory M2 phenotype. The method can comprises providing a composition comprising a recombinant adeno-associated virus (rAAV) vector comprising an exogenous gene encoding ApoA-I Milano or a fragment thereof, and administering the composition to a mammal in need thereof to change the phenotype of monocytes or macrophages from a proinflammatory M1 phenotype to an anti-inflammatory M2 phenotype. By changing the phenotype of monocytes or macrophages from a proinflammatory M1 phenotype to an anti-inflammatory M2 phenotype, atherosclerosis can be treated. The present invention also describes a method of monitoring macrophage phenotypic switching and a method of assessing the efficacy of the treatment of atherosclerosis.

Abstract: The invention relates to the discovery that mutations of serine residues of an AAV capsid results in significantly greater transfection efficiency than the wild type AAV2 virus. In one embodiment, the present invention provides a method of improving efficiency of gene transfer and/or gene therapy to a cell by inhibiting phosphorylation of one or more serine residues of a virus capsid protein, where the inhibition of the phosphorylation of one or more serine residues results in a decrease of ubiquitination of the virus capsid protein in the cell. In another embodiment, one of the one or more serine residues is Serine 264. In another embodiment, the Serine 264 residue is mutated to Alanine (S 264 A).

Abstract: The invention relates to the isolation and use of hematopoietic and embryonic stem cells. Additionally, the inventors identified the peritoneal cavity as a new source of hematopoietic stem cells. In one embodiment, the invention provides methods of isolating progenitor and/or stem cells from the peritoneal cavity. In another embodiment, the invention provides methods of transporting progenitor and/or stem cells from the peritoneal cavity to another organ. In another embodiment, the present invention provides methods of regenerating bioengineered tissues and/or reconstituting an hematopoietic system.

Abstract: A method of changing the phenotype of monocytes and macrophages from a pro inflammatory MI phenotype to an anti-inflammatory M2 phenotype is disclosed. The method can comprises providing a composition comprising a recombinant adeno-associated virus (rAAV) vector comprising an exogenous gene encoding ApoA-1 Milano or a fragment thereof, and administering the composition to mammal in need thereof to change the phenotype of monocytes or macrophages from a pro inflammatory M1 phenotype to an anti inflammatory M2 phenotype. By changing the phenotype of monocytes or macrophages from a pro-inflammatory M1 phenotype to anti-inflammatory M2 phenotype, atherosclerosis can be treated. A method of monitoring macrophage phenotypic switching and a method of assessing the efficacy of the treatment of atherosclerosis are also described.

Abstract: The invention relates to the discovery that mutations of serine residues of an AAV capsid results in significantly greater transfection efficiency than the wild type AAV2 virus. In one embodiment, the present invention provides a method of improving efficiency of gene transfer and/or gene therapy to a cell by inhibiting phosphorylation of one or more serine residues of a virus capsid protein, where the inhibition of the phosphorylation of one or more serine residues results in a decrease of ubiquitination of the virus capsid protein in the cell. In another embodiment, one of the one or more serine residues is Serine 264. In another embodiment, the Serine 264 residue is mutated to Alanine (S 264 A).

Abstract: The invention relates to the isolation and use of hematopoietic and embryonic stem cells. Additionally, the inventors identified the peritoneal cavity as a new source of hematopoietic stem cells. In one embodiment, the invention provides methods of isolating progenitor and/or stem cells from the peritoneal cavity. In another embodiment, the invention provides methods of transporting progenitor and/or stem cells from the peritoneal cavity to another organ. In another embodiment, the present invention provides methods of regenerating bioengineered tissues and/or reconstituting an hematopoietic system.

Abstract: The invention disclosed herein relates to the detection or diagnosis of atherosclerosis by measuring the level of the protein eotaxin in an individual's serum. The presence of eotaxin above levels specified herein is indicative that atherosclerosis may be present. Detection of elevated eotaxin levels in serum may provide a means to diagnose atherosclerosis prior to the onset of symptoms.

Abstract: Described herein are methods for transdifferentiating monocytes/macrophages into endothelial cells, based on the inventors' identification of pleiotrophin (“PTN”) as the gene responsible for this transdifferentiation. Further described are therapeutic methodologies for the promotion or inhibition of neovasculanization based on modulation of PTN.