Přejít k obsahu
Merck

Sca-1 knockout impairs myocardial and cardiac progenitor cell function.

Circulation research (2012-07-18)
Brandi Bailey, Jenna Fransioli, Natalie A Gude, Roberto Alvarez, Xiaoxue Zhang, Åsa B Gustafsson, Mark A Sussman
ANOTACE

Cardiac progenitor cells are important for maintenance of myocardial structure and function, but molecular mechanisms governing these progenitor cells remain obscure and require elucidation to enhance regenerative therapeutic approaches. To understand consequences of stem cell antigen-1 (Sca-1) deletion on functional properties of c-kit+ cardiac progenitor cells and myocardial performance using a Sca-1 knock-out/green fluorescent protein knock-in reporter mouse (ScaKI). Genetic deletion of Sca-1 results in early-onset cardiac contractile deficiency as determined by echocardiography and hemodynamics as well as age-associated hypertrophy. Resident cardiac progenitor cells in ScaKI mice do not respond to pathological damage in vivo, consistent with observations of impaired growth and survival of ScaKI cardiac progenitor cells in vitro. The molecular basis of the defect in ScaKI cardiac progenitor cells is associated with increased canonical Wnt signaling pathway activation consistent with molecular characteristics of lineage commitment. Genetic deletion of Sca-1 causes primary cardiac defects in myocardial contractility and repair consistent with impairment of resident cardiac progenitor cell proliferative capacity associated with altered canonical Wnt signaling.

MATERIÁLY
Číslo produktu
Značka
Popis produktu

Sigma-Aldrich
β-Catenin/Tcf Inhibitor, FH535, The β-Catenin/Tcf Inhibitor, FH535, also referenced under CAS 108409-83-2, controls the biological activity of β-Catenin/Tcf. This small molecule/inhibitor is primarily used for Cell Signaling applications.