by Amy Adams on February 17, 2009 at 12:03PM | comments
Researchers at the Gladstone Institute of Cardiovascular Disease may have discovered why developing heart muscles cells multiply in numbers while the adult counterparts do not. This finding could lead to therapies that roll back the clocks on heart muscle cells after injury such as a heart attack, allowing those cells to multiply and repair the damage. The researchers specifically looked at the role of cells called fibroblasts, which are packed in the heart amidst the muscle cells.
by Amy Adams on November 12, 2008 at 11:46AM | comments
Researchers at the Gladstone Institute for Cardiovascular Disease found a genetic factor that helps in the earliest stages of heart development as the primitive tube loops around on itself and forms the separate chambers. This factor -- a short relative of DNA called microRNA -- has an identical counterpart in humans, leading the researchers to believe that their work in fish is likely to relate directly to human heart development.
by Amy Adams on October 22, 2008 at 11:47AM | comments
Researchers at the Stanford University School of Medicine found that cells derived from human embryonic stem cells could repair damage in a mouse model of heart attack. The researchers first looked at which genes were active at every stage between the human embryonic stem cells and early heart muscle cells. The cells they implanted mirrored the genes that are active in the hearts of 20 week old fetal mice.
by Amy Adams on March 6, 2008 at 11:08AM | comments
Researchers at the Gladstone Institute for Cardiovascular Disease discovered how two specific tiny genetic factors called microRNAs influence the differentiation of embryonic stem cells into heart muscle. They found that the factors not only drive the versatile cells to become heart, but also actively prevent them from becoming other tissue such as bone adding to their potential to make therapy more specific and targeted for patients.
by Amy Adams on February 15, 2008 at 11:21AM | comments
Researchers at UC, Irvine used mouse embryonic stem cells to demonstrate that a specific mutation can cause cardiomyopathy, with a thickened heart wall, in the mouse. The team looked at the small DNA molecule located outside of the nucleus, so-called mitochondrial DNA, which we all inherit exclusively from our mothers. They also discovered that severe mutations in this mitochondrial DNA are readily eliminated from the mouse germ line in just four generations. They expect the method they used to become a robust research tool to study the impact of mutations on stem cells.