Abstract
The molecular motor which traffics epithelial sodium channels (ENaC) to and from the apical membrane is still unknown. We hypothesized that myosins, specifically Myosin 5 (Myo5), is involved in ENaC exocytosis. To determine the role of Myo5 in ENaC trafficking, we knocked down Myo5a and Myo5c in mCCD cells using shRNAs. We then measured the short-circuit current (Isc) and membrane capacitance change (ΔCT) of cells in Ussing chambers before and following cAMP activation. The Isc and CT change following cAMP-induced trafficking in knockdowns was significantly smaller than mCCD controls. Cells with Myo5c knocked down had a ΔIsc of 2.9 μA ± 1.03 μA compared to controls ΔIsc of 4.7 μA ± 0.68μA. There was a significant reduction in ΔCT (21% for controls vs. 14% in Myo5c) following cAMP stimulation. No significant change in Isc or CT response was observed for Myo5a knockdowns. There was no significant difference in basal (unstimulated) Isc between controls and Myo5c knockdowns. These results suggest that Myo5c is specifically involved in cAMP-induced ENaC trafficking to the apical membrane in response to cAMP stimulation and not constitutive ENaC protein turnover.
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