Background
ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) is a recently identified family of extracellular metalloproteinases that has been shown to participate in tissue destruction. We hypothesized that ADAMTS-1 and ADAMTS-4 expression is increased in aortic tissues from patients with thoracic aortic aneurysms and dissections.
Methods
We examined ADAMTS-1 and ADAMTS-4 expression in human descending thoracic aortic aneurysms (n=14), chronic descending thoracic aortic dissections (n=16), and descending thoracic aortas from age-matched control organ donors (n=12). In these tissues, we also evaluated the degradation of versican, a proteoglycan substrate of ADAMTS-1 and ADAMTS-4. In cultured macrophages, we examined whether ADAMTS-4 functions in macrophage infiltration by using a transwell assay.
Results
ADAMTS-1 and ADAMTS-4 protein and mRNA expression was significantly higher in thoracic aortic aneurysm and dissection tissues than in control aortic tissues. Double immunofluorescence staining showed the expression of ADAMTS-1 and ADAMTS-4 in smooth muscle cells and macrophages. Consistent with the upregulation of ADAMTS-1 and ADAMTS-4 in thoracic aortic aneurysm and dissection tissues, versican was degraded significantly more in these tissues than in control aortic tissues. In cultured macrophages, transforming growth factor-β increased ADAMTS-4 protein levels and induced macrophage invasion; knocking down ADAMTS-4 reduced cell invasion.
Conclusions
Increased expression of ADAMTS proteins may promote thoracic aortic aneurysm progression by degrading versican and facilitating macrophage invasion.
INTRODUCTION: Extended Focussed Assessment with Sonography for Trauma (eFAST) has increasingly become the standard of care to identify hemo/pneumothorax, with a much greater sensitivity than a supine CXR (87% vs. 46%). Pneumothorax is recognized as a result of no "lung sliding", which occurs because the visceral and parietal pleural linings have separated. Symptomatic pneumothoraces are treated with tube thoracotomy. CASE PRESENTATION: 65 year old male presented to the trauma center after blunt chest trauma and hypotension. CXR did not show any obvious pathology, but eFAST failed to show any lung slide on the left chest. A left sided tube thoracotomy was performed after 1500mL of frank blood was initially evacuated; the entire lung was noted to be densely adherent to the chest wall; hemorrhage control was obtained by performing a pulmonary tractotomy/lobectomy of the involved lung segment, and the patient was then transferred to the SICU for ongoing resuscitation.
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