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1C (CaV1.2) L-type calcium channel
mediates mechanosensitive calcium regulation
Enteric NeuroScience Program and 1 Division of Gastroenterology and Hepatology, 2 Department of Physiology and Biophysics, Mayo Clinic, Rochester, Minnesota 55905
Smooth muscle exhibits
mechanosensitivity independent of neural input, suggesting that
mechanosensitive pathways reside within smooth muscle cells. The native
L-type calcium current recorded from human intestinal smooth muscle is
modulated by stretch. To define mechanosensitive mechanisms involved in
the regulation of smooth muscle calcium entry, we cloned the
1C L-type calcium channel subunit (CaV1.2)
from human intestinal smooth muscle and expressed the channel in a
heterologous system. This channel subunit retained mechanosensitivity
when expressed alone or coexpressed with a 
2 calcium
channel subunit in HEK-293 or Chinese hamster ovary cells. The
heterologously expressed human cardiac 1C splice form
also demonstrated mechanosensitivity. Inhibition of kinase signaling
did not affect mechanosensitivity of the native channel. Truncation of the 1C COOH terminus, which contains
an inhibitory domain and a proline-rich domain thought to mediate
mechanosensitive signaling from integrins, did not disrupt
mechanosensitivity of the expressed channel. These data demonstrate
mechanical regulation of calcium entry through molecularly identified
L-type calcium channels in mammalian cells and suggest that the
mechanosensitivity resides within the pore forming
1C-subunit.
smooth muscle; mechanogated; voltage gated
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