Abstract
Proper control of multipotent/stem cell number and fate is essential for ensuing organ formation during development. β1-integrin, a subfamily of cell surface receptors, has a conserved role in maintenance of multipotent/stem cells, including renal progenitor cells, follicle stem cells, epidermal stem cells and neural stem cells. However, it remains unclear whether β1-integrin has a role in cardiac progenitor cell (CPC) development. Here we show that a mesodermal deletion of β1-integrin decreases Isl1+ cell number in the second pharyngeal arch (PA2), where CPCs undergo renewal and expansion. Mesp1 lineage-specific mosaicism revealed that β1-integrin-deleted Isl1+ cells do not proliferate in the PA2. Consistently, β1-integrin-deleted Isl1+ CPCs failed to expand in vitro, independent of PA2 cells. β1-integrin co-localized and physically associated with Numb, a crucial regulator of CPC renewal and expansion. Importantly, Numb/Numbl-deleted CPCs showed dramatic reduction in β1-integrin levels. These findings suggest that β1-integrin is a key mediator of the Numb pathway in CPC maintenance.
Original language | English (US) |
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Pages (from-to) | 256-260 |
Number of pages | 5 |
Journal | Biochemical and Biophysical Research Communications |
Volume | 500 |
Issue number | 2 |
DOIs | |
State | Published - Jun 2 2018 |
Keywords
- Cardiac development
- Cardiac progenitor expansion
- ES/iPS cells
- Numb/Numbl
- Second heart field
- β1-integrin
ASJC Scopus subject areas
- Biophysics
- Biochemistry
- Molecular Biology
- Cell Biology