JOURNAL ARTICLE
Analysis of c-myc, PAI-1 and uPAR in patients with incisional hernias.
BACKGROUND: Disturbed wound healing leading to alterations in collagen composition has been thought to play a key role in the pathogenesis of incisional hernia formation. The aim of the present study was to further characterise the scarring process in such patients.
METHODS: Mature skin scars from patients with either primary or recurrent incisional hernias were compared to mature abdominal skin scars from patients without hernias. The distribution of collagen types I and III was analysed using crosspolarisation microscopy. Expression of c-myc--a parameter for cell differentiation and proliferation--and of PAI-1 and uPAR--parameters of the proteolytic cascade in wound healing--were determined by immunohistochemistry.
RESULTS: In agreement with previous studies, decreased collagen I/III ratios were found in patients with incisional hernias. In these patients, c-myc levels were significantly elevated whereas plasminogen activator inhibitor-1 (PAI-1) and urokinase-plasminogen activator receptor (uPAR) levels were only slightly increased. In contrast to controls, a significant correlation between c-myc, PAI-1 and uPAR expression and collagen I/III ratios was found in patients with incisional hernias.
CONCLUSION: The differential correlation of collagen types and expression of c-myc, PAI-1 and uPAR within the scar tissue might represent a causal factor in incisional hernia formation.
METHODS: Mature skin scars from patients with either primary or recurrent incisional hernias were compared to mature abdominal skin scars from patients without hernias. The distribution of collagen types I and III was analysed using crosspolarisation microscopy. Expression of c-myc--a parameter for cell differentiation and proliferation--and of PAI-1 and uPAR--parameters of the proteolytic cascade in wound healing--were determined by immunohistochemistry.
RESULTS: In agreement with previous studies, decreased collagen I/III ratios were found in patients with incisional hernias. In these patients, c-myc levels were significantly elevated whereas plasminogen activator inhibitor-1 (PAI-1) and urokinase-plasminogen activator receptor (uPAR) levels were only slightly increased. In contrast to controls, a significant correlation between c-myc, PAI-1 and uPAR expression and collagen I/III ratios was found in patients with incisional hernias.
CONCLUSION: The differential correlation of collagen types and expression of c-myc, PAI-1 and uPAR within the scar tissue might represent a causal factor in incisional hernia formation.
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