Distribution and Compartmentalization of Contractile Proteins Following Traumatic Brain Injury

Calponin (Cp) and caldesmon (Cd) are actin-binding proteins involved in the regulation of smooth muscle (SM) tone during blood vessel contraction. While in vitro studies have reported modifications of these proteins during vessel contractility, their role in vivo remains unclear. Traumatic brain injury (TBI) causes disruption of cerebral microvascular tone, leading to sustained contractility in reacting microvessels and cerebral hypoperfusion. This study aimed to determine the spatial and temporal expressions of Cp and Cd in rat cerebral cortical and hippocampal microvessels post TBI. Reacting microvessels were analyzed in control, 4, 24, and 48 hours post injury. Single and double immunocytochemical techniques together with semiquantitative analyses revealed an upregulation of Cp in SM at all time frames post TBI; with the protein migrating from the luminal face of SM to the abluminal wall. Similarly, Cd expression significantly increased in both SM and endothelial cells (En). However, while Cd in SM remained elevated, expression levels in En returned to normal at 48 hours post TBI. The results suggest that Cp and Cd levels increase following TBI while compartmentalizing to specific subcellular domains. These changes are temporally associated with modifications in the cytoskeleton and contractile apparatus of SM and En during blood vessel contractility. Furthermore these changes may underlie the state of sustained contractility and hypoperfusion observed in reacting microvessels after TBI.