Subcellular redistribution of calponin underlies sustained vascular contractility following traumatic brain injury

The purpose of this study was to observe temporal changes in calponin (Cp), a contractile protein, in response to traumatic brain injury (TBI).

Double immunocytochemistry in conjunction with morphometric methods was used to study Cp temporal migration in smooth muscle cells (SM) of reacting microvessels following TBI, as induced using a weight-drop, acceleration impact method.

Quantification of migrated Cp in the SM wall after TBI was carried out on three-dimensional orthographic reconstructions of serial, digitally acquired images and optical densitometry. Color shifts in Cp intensity were measured in three arbitrary longitudinal compartments, luminal (lu), middle (m) and abluminal (ablu), of SM cytoplasm with respect to proximity to the vessel's lumen. By 24 and 48 hours after TBI, most Cp had migrated from the SM compartment closest to the lu to that farthest away or ablu. In addition, a qualitative increase in Cp was detected closest to the ablu compartment in those segments of the vessel severely constricted.

Cp migration from cytoskeletal to contractile regions of SM supports its role both in the initiation of vessel contractility and its interaction with cytoskeletal structures subjacent to the cell membrane in SM's contracted state.