β-Catenin, a key regulator of barrier integrity, is an important component of the adherens junctional complex. Although the roles of β-catenin in maintaining the adherens junctions and Wnt signaling are known, the dynamics of β-catenin following insult and its potential role in vascular recovery/repair remain unclear. Our objective was to define β-catenin's dynamics following disruption of the adherens junctional complex and subsequent recovery. Rat lung microvascular endothelial cells were treated with active caspase 3 enzyme, by protein transference method, as an inducer of junctional damage and permeability. The disruption and subsequent recovery of β-catenin to the adherens junctions were studied via immunofluorescence. Rat lung microvascular endothelial cell monolayers were used to measure hyperpermeability. To understand the role of β-catenin on nuclear translocation/transcriptional regulation in relationship to the recovery of the adherens junctions, Tcf-mediated transcriptional activity was determined. Active caspase 3 induced a loss of β-catenin at the adherens junctions at 1 and 2 h followed by its recovery at 3 h. Transference of Bak peptide, an inducer of endogenous caspase 3 activation, induced hyperpermeability at 1 h followed by a significant decrease at 2 h. Inhibition of GSK-3β and the transfection of β-catenin vector increased Tcf-mediated transcription significantly (P < 0.05). The dissociated adherens junctional protein β-catenin translocates into the cytoplasm, resulting in microvascular hyperpermeability followed by a time-dependent recovery and relocation to the cell membrane. Our data suggest a recycling pathway for β-catenin to the cell junction.