An in vivo model was used to investigate the role of
cathepsins in mouse intestine after mechanical manipulation. Inspection of different intestine segments by immunofluorescence microscopy provided evidence for a local release of
cathepsin B from cells of individual gut sections shortly after traumatic injury. Densitometry of immunoblots ruled out alterations in
cathepsin B expression levels. Because similar results were obtained with both mouse and rat intestine
trauma models, we were interested in identifying potential targets of released
cathepsin B in early post-traumatic phases. Immunoblotting revealed initial declines followed by an increase in
protein levels of
claudin-1 and
E-cadherin, indicating that tight junctions and cell-cell adhesions were only transiently compromised by surgical
trauma. Apical
aminopeptidase N and
dipeptidyl peptidase IV were only slightly affected, whereas basolateral
low-density lipoprotein receptors were strongly up-regulated in response to
trauma. As potential targets of
cathepsin B released from injured cells, we identified
collagen IV and
laminin of the basement membrane that was damaged during initial post-traumatic stages. Because increased
collagen IV expression was observed in the intestine of
cathepsin B-deficient animals, we propose a direct role of
cathepsin B in that it contributes to acute post-traumatic extracellular matrix damage and may thereby facilitate onset of post-operative
ileus.