Subjecting nonbeating cardiac myocytes to a 5% static stretch for 24 hours increased beta 1-integrin by 21% and vinculin by 39%, indicating mechanical forces stabilize these cellular levels.
Do mechanical forces regulate focal adhesion and costamere assembly in cardiac myocytes?
Mechanical forces stabilize cellular levels of beta 1-integrin and vinculin, regulating their association with focal adhesions and costameres in cardiac myocytes.
To determine whether the formation and maintenance of focal adhesions and costameres in cardiac myocytes are influenced by the mechanical forces that they transmit, we mechanically unloaded these cells by inhibiting their spontaneous contractile activity with the calcium-channel blocker nifedipine (12 microM). Interference-reflection and fluorescence microscopy revealed that within 24 h of arrest, beta 1-integrin- and vinculin-positive focal adhesions and costameres were disrupted. Loss of mature beta 1-integrin from the cell surface was observed in cell surface-labeling experiments and in Western blots. Subjecting nonbeating cells to a 5% static stretch for 24 h resulted in an increase of 21% for beta 1-integrin and 39% for vinculin. Stretching beating cells resulted in 71 and 9% increases, respectively. Intracellular concentrations of pre-beta 1 were not affected by contractile activity or by stretch. Our results indicate that mechanical forces stabilize the cellular levels of beta 1-integrin and vinculin by possibly regulating their association with the formation and maintenance of focal adhesions and costameres.
Sharp et al. (Fri,) conducted a other in Cardiac myocytes (in vitro). Mechanical unloading (nifedipine) and static stretch vs. Spontaneous contractile activity / non-stretched cells was evaluated on Levels of beta 1-integrin and vinculin, and focal adhesion/costamere assembly. Subjecting nonbeating cardiac myocytes to a 5% static stretch for 24 hours increased beta 1-integrin by 21% and vinculin by 39%, indicating mechanical forces stabilize these cellular levels.