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On December 18, 2018, the international academic journal Circulation published online in the form of Research Letter the results of the Research Group's Research Group, "Fate Mapping of Sca1 Sca1, Cardiac Progenitor Cells in The Adult Mouse Hearts".
in this work, the researchers used Sca1-2A-CreER mice that specifically label edtaps the heart Sca1-plus stem cells to reveal that Sca1 plus heart stem cells can be differentiated into cardiac endothelial cells and fibroblasts in normal physiological and heart damage models, not into myocardial cells.
the study reveals the trans-differentiation potential of Sca1 plus heart stem cells, which will help researchers gain a better understanding of the role of Sca1 plus stem cells in adult hearts and provide new ideas for cardiovascular regenerative medicine research.
coronary artery disease causes myocardial infarction and heart failure, which is the leading cause of death from disease in humans. After the death of acute myocardial infarction in
, a large number of myocardial cells and vascular endothelial cells died, only a small number of myocardial cell division and proliferation, how to improve the regeneration of heart muscle cell has become a hot research topic in this field.
early studies have shown that heart stem cells present in the heart can contribute to myocardial cells in the event of damage, thereby improving the ability to repair the damaged heart.
, in vitro cells and transplantation experiments show that Sca1 plus heart stem cells can be differentiated into heart muscle cells, while Sca1 plus as vascular stem cells can be transformed into vascular endothelial cells through proliferation and differentiation.
, Sca1 plus has a variety of differentiation potentials, but whether the endogenous Sca1 plus cells in the heart can contribute to myocardial cells and endothelial cells needs further study.
illustration: Sca1 plus heart stem cells cannot be differentiated into myocardial cells in the O-V. Injury Model (O-V) and the Osmytoris Reperfusion Model (W-X).
in the case of cardiac stability and damage, Sca1 plus heart stem cells have the potential to be converted into endothelial and fibroblasts, but not to myocardial cells (Y).
to systematically study the changes in the fate of adult Sca1 plus heart stem cells in normal physiological and heart damage conditions, the researchers established a specific marker Sca1 plus heart stem cell genealogy tracing system, anti-estrogen drug tamoxifen induction treatment 24-48 hours later, collected sample tests found Sca1-2A-CreER; R26-tdTomato mice can specifically and efficiently label Sca1 plus heart stem cells, which mainly label vascular endothelial cells and a small number of fibroblasts.
using this specific mouse, the researchers tested the transdifferentiation of Sca1-plus heart stem cells in physiological conditions and myocardial infarction.
pass edper sca1-2A-CreER at 8 weeks; R26-tdTomato mice injected tamoxifen, collected 1-12 weeks after injection of mouse heart samples, tests found that in the steady state of the heart, Sca1 plus heart stem cells can contribute to the heart endothelial cells and a small number of fibroblasts, but can not differentiate myocardial cells.
further experiments, the researchers in tamoxifen-induced Sca1-2A-CreER; A model of heart injury was carried out in R26-tdTomato mice, including a model of myocardial infarction, ischemia reperfusion of the heart.
researchers found that in the heart damage model, Sca1 plus heart stem cells can contribute to vascular endothelial cells and fibroblasts without switching to myocardial cells.
the above results show that adult Sca1 plus heart stem cells have the potential to transdifferentiate into vascular endothelial cells and fibroblasts, and promote cardiac repair through vascular rebirth.
journal, which published a special review of the work and sca1 stem cell-related work in the same period, which he said revealed the fate of Sca1 heart stem cells in adult mammals and contributed to the development and advancement of the heart stem cell field.
the work was completed by postdoctoral researcher Tang Wei and others, and received strong support from Professor Yu Yu of the Chinese Academy of Medical Sciences, Professor Hu Shengshou of the University of Chinese of Hong Kong, Professor Lu Ailan of the University of Chinese of Hong Kong and researcher Qing-Dong Wang of AstraZeneca, and also received financial support from the Chinese Academy of Sciences, the State Fund Committee, the State Ministry of Science and Technology, and the Shanghai Science and Technology Commission.
Source: Institute of Biochemistry and Cell Biology.