Open AccessFate of undifferentiated mouse embryonic stem cells within the rat heart: role of myocardial infarction and immune suppression
Author(s) -
He Qing,
Trindade Pedro T.,
Stumm Michael,
Li Jian,
Zammaretti Prisca,
Bettiol Esther,
DuboisDauphin Michel,
Herrmann François,
Kalangos Afksendyios,
Morel Denis,
Jaconi Marisa E.
Publication year - 2009
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/j.1582-4934.2008.00323.x
Subject(s) - embryonic stem cell , stem cell , biology , transplantation , microbiology and biotechnology , cardiac function curve , immune privilege , immune system , paracrine signalling , myocardial infarction , medicine , immunology , cancer research , heart failure , receptor , biochemistry , gene
It has recently been suggested that the infarcted rat heart microenvironment could direct pluripotent mouse embryonic stem cells to differentiate into cardiomyocytes through an in situ paracrine action. To investigate whether the heart can function as a cardiogenic niche and confer an immune privilege to embryonic stem cells, we assessed the cardiac differentiation potential of undifferentiated mouse embryonic stem cells (mESC) injected into normal, acutely or chronically infarcted rat hearts. We found that mESC survival depended on immunosuppression both in normal and infarcted hearts. However, upon Cyclosporin A treatment, both normal and infarcted rat hearts failed to induce selective cardiac differentiation of implanted mESC. Instead, teratomas developed in normal and infarcted rat hearts 1 week and 4 weeks (50% and 100%, respectively) after cell injection. Tight control of ESC commitment into a specific cardiac lineage is mandatory to avoid the risk of uncontrolled growth and tumourigenesis following transplantation of highly plastic cells into a diseased myocardium.