Abstract: The present invention generally provides methods for administering a composition having an ILK-based protein or peptide having a sequence that is at least 90% homologous to wild-type human integrin-linked kinase (ILK) protein for use in treating or administering to cardiac cells in vitro or in vivo. The ILK-based protein or peptide may further have a mutation or substitution at a position corresponding to amino acid position 211 of wild-type human ILK replacing the arginine (R) with an alanine (A). The present invention further provides compositions having polynucleotides encoding such proteins or peptides. Various vectors, delivery reagents and the like are also provided for use in delivering the compositions to cells. The compositions administered to cells in vitro or in vivo according to present methods may be used to treat, prevent, etc., heart failure, ischemic disease, cardiomyopathy, etc.

Abstract: Modulation of the integrin-linked kinase (ILK) signaling pathway is used to enhance the remodeling process relevant to a wide range of cardiac diseases. More specifically, a process to instigate beneficial human cardiac hypertrophy or for post myocardial infraction (MI) remodeling comprising illiciting an overexpression of ILK, is described. The ILK signaling pathway is also used as a means for cardiac stem cell proliferation and self-renewal.

Abstract: Modulation of the integrin-linked kinase (ILK) signaling pathway is used to enhance the remodeling process relevant to a wide range of cardiac diseases. More specifically, a process to instigate beneficial human cardiac hypertrophy or for post myocardial infraction (MI) remodeling comprising illiciting an overexpression of ILK, is described. The ILK signaling pathway is also used as a means for cardiac stem cell proliferation and self-renewal.

Abstract: The present invention generally provides methods for administering a composition having an ILK-based protein or peptide having a sequence that is at least 90% homologous to wild-type human integrin-linked kinase (ILK) protein for use in treating or administering to cardiac cells in vitro or in vivo. The ILK-based protein or peptide may further have a mutation or substitution at a position corresponding to amino acid position 211 of wild-type human ILK replacing the arginine (R) with an alanine (A). The present invention further provides compositions having polynucleotides encoding such proteins or peptides. Various vectors, delivery reagents and the like are also provided for use in delivering the compositions to cells. The compositions administered to cells in vitro or in vivo according to present methods may be used to treat, prevent, etc., heart failure, ischemic disease, cardiomyopathy, etc.

Abstract: Modulation of the integrin-linked kinase (ILK) signaling pathway is used to enhance the remodeling process relevant to a wide range of cardiac diseases. More specifically, a process to instigate beneficial human cardiac hypertrophy or for post myocardial infarction (MI) remodeling comprising illiciting an overexpression of ILK, is described. The ILK signaling pathway is also used as a means for cardiac stem cell proliferation and self-renewal.

Abstract: The invention relates to a process for identification, amplification and differentiation of cardiac stem cells by utilizing an ILK based protocol. The invention further relates to a process for post myocardial infarction (IVII) remodeling by way of the integrin linked kinase (ILK) signaling pathway. Still further, the invention relates to a process for affecting an ability to control and/or manipulate stem cell frequency, cellular fate, self-renewal, multilineage differentiation, and potential for oncogenesis in cardiac tissue derived from embryonic stem cells, fetal tissue or adult tissue comprising modulation of ILK signaling amplification whereby stem cell renewal and expansion results.

Abstract: Modulation of the integrin-linked kinase (ILK) signaling pathway is used to enhance the remodeling process relevant to a wide range of cardiac diseases. More specifically, a process for mediating a broadly adaptive form of human cardiac hypertrophy and a protective process for post myocardial infarction (MI), both comprising illiciting an overexpression of ILK, are described. Upregulation of ILK is also used in a process for affecting ILK mediated reduction of infarct size and beneficial increase in the left ventricular mass post MI.

Abstract: Modulation of the integrin-linked kinase (ILK) signaling pathway is used to enhance the remodeling process relevant to a wide range of cardiac diseases. More specifically, a process to instigate beneficial human cardiac hypertrophy or for post myocardial infarction (MI) remodeling comprising illiciting an overexpression of ILK, is described.

Abstract: The present invention is directed toward elucidation of a human fetal gene expression program in response to simulated ischemia/reperfusion (I/R) in order to identify molecular targets which account for the innate cardioprotection exhibited by the fetal phenotype.

Abstract: The present invention is directed toward identification of cardioprotective gene programs in the neonatal heart. Specifically, the newborn (immature) heart or alternatively fetal heart has been recognized as having an increased resistance to pathophysiological forms of stress, e.g. hypoxic stress. The pattern of gene expression in immature heart subject to naturally occurring hemodynamic and hypoxic stress, e.g. that associated with obstructive congenital heart disease, is herein revealed by differential gene profiling; and the induction of a cardioprotective gene pattern, and particularly useful subsets thereof, in the heart chronically adapted to stress is confirmed. Thus, the chronically stressed immature heart provides a novel biosynthetic platform for cardioprotective gene expression, useful as a basis for the development of diagnostic and therapeutic modalities.

Abstract: Reactivity between an alloantigen and an anti-alloantigen is indicative of immunological reactivity between two biological samples of the same species. Reactivity between a xenoantigen and an anti-xenoantigen is indicative of immunological reactivity between two biological samples of different species. In many cases both of the reactions are indicative of an antibody-mediated rejection. Anti-antibodies can be employed to reduce cross-reactivity in many transplantation-type situations, either within a similar species, or across species lines. These anti-antibodies are prepared against the antibodies responsible for the antibody-mediated rejection. These anti-antibodies can then be used in vivo or in vitro to complex with the antibodies thus reducing or eliminating reactivity between an alloantigen and an anti-alloantigen or reactivity between a xenoantigen and an anti-xenoantigen between any two species combinations.