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Abstract
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 h post-injury. Single and double
immunocytochemical techniques together with semiquantitative analyses revealed a Cp
upregulation in SM at all time frames post-TBI; with the protein migrating from SM
cytosol to the vicinity of the cell membrane. Similarly, Cd immunoreactivity significantly
increased in both SM and endothelial cells (En). However, while Cp and Cd in SM remained
elevated, their levels in En returned to normal at 48 h post-TBI. The results suggest
that Cp and Cd levels increase 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.