These microscopy images demonstrate the effects of Notch signalling on the hearts of newborn mice (top) and of adult mice after a heart attack (bottom). In a normal neonatal heart (top left), the two major heart chambers (ventricles) are clearly separated by tissue (septum). But when Notch signalling was inactivated in an embryo’s heart muscle cells, the septum between the ventricles of the newborn mouse’s heart was incomplete (asterisk). The same defect commonly occurs in humans with congenital heart disease, often leading to circulatory distress. In the images of adult hearts (bottom), healthy tissue is shown in red and damaged tissue in blue. Normally (bottom left), a heart attack causes extensive tissue damage to the left ventricle (right-hand cavity), but mice in which Notch was re-activated after the heart attack had reduced tissue damage (bottom right) and improved cardiac function.
Image credit: EMBL
(Source: embl.de)
These microscopy images demonstrate the effects of Notch signalling on the hearts of newborn mice (top) and of adult mice after a heart attack (bottom). In a normal neonatal heart (top left), the two major heart chambers (ventricles) are clearly separated by tissue (septum). But when Notch signalling was inactivated in an embryo’s heart muscle cells, the septum between the ventricles of the newborn mouse’s heart was incomplete (asterisk). The same defect commonly occurs in humans with congenital heart disease, often leading to circulatory distress. In the images of adult hearts (bottom), healthy tissue is shown in red and damaged tissue in blue. Normally (bottom left), a heart attack causes extensive tissue damage to the left ventricle (right-hand cavity), but mice in which Notch was re-activated after the heart attack had reduced tissue damage (bottom right) and improved cardiac function.
Image credit: EMBL
(Source: embl.de)
Posted 3 months ago & Filed under heart, microscope, mutation, science, mice, embryo, 120 notes View high resolution
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