Time-dependent expression of ICAM-1 & VCAM-1 on coronaries of the heterotopically transplanted mouse heart

To investigate the pathogenesis of accelerated graft atherosclerosis after rdiac transplantation, a genetically well-defined and reproducible animal del is required. We performed heterotopic intraabdominal heart transplantation tween the two inbred strains of mice. Forty hearts from B10.A mice were ansplanted into B10.BR mice. Recipients were sacrificed at 1, 3, 5, 7, 14, 28, d 42 days after implantation. The specimens from both donor and recipient were amined with fluorescent immunohistochemistry and the serial histopathologic anges were evaluated. In the donor hearts, ICAM-1 and VCAM-1 expressions were nimal at day 1 and they gradually increased, reaching their peaks on day 5 or and remained unchanged by day 42. However, there were very little expressions the recipients' hearts. Mean percent areas of intima in the donor coronaries vealed progressive increase by day 42. However, those in the recipients cupied consistently less than 5% of the lumen. In conclusion, we demonstrated at a heterotopic murine heart transplantation model was a useful tool to oduce transplantation coronary artery disease and that adhesion molecules on e cardiac allografts were activated very early and remained elevated at all me-points, nonetheless the arterial lesion was detected after day 28 and its ogression was accelerated thereafter.

Effect of angiopeptin and aspirin on accelerated graft atherosclerosis in transplanted mouse heart

In this study of the inhibitory effects of angiopeptin and aspirin on the development of accelerated graft atherosclerosis (AGAS), 22 B10.BR mice received intra-abdominal heterotopic heart transplants from B10.A mice, without immunosuppression. Group 1 (n = 5) received no pharmacological intervention, Group 2 (n = 6) was treated with angiopeptin, Group 3 (n = 5) with aspirin, and Group 4 (n = 6) with both. There was no significant difference in the incidence of AGAS among these groups. The magnitude of intimal lesion development showed less narrowing of large vessels (> 100 microns in diameter) in groups 2 and 4--i.e. the groups received angiopeptin (Group 1 = 46.9 +/- 9.3%, Group 2 = 28.5 +/- 9.2%, Group 3 = 44.1 +/- 10.9%, Group 4 = 24.2 +/- 5.9%; p < 0.01). Comparison of the fraction of tropomyosin-positive staining cells in the intima revealed a lesser degree of staining in Group 2 (p < 0.01). No intervention was effective in preventing smooth muscle cell proliferation in the media or inflammatory cell infiltration in the adventitia. In conclusion, our data suggest that angiopeptin is effective in the direct inhibition of intimal smooth muscle cell proliferation in relatively large vessels, whereas aspirin exhibits no inhibitory role in the progression of AGAS. Angiopeptin appears to be a potential therapeutic agent for inhibiting the progression of postoperative AGAS in clinical heart transplantation.

Clinical Features and Molecular Diagnosis of CATCH-22 Syndrome

BACKGROUND: CATCH-22 syndrome is a common genetic disorder with features of cardiac defect, abnormal face, thymic hypoplasia, cleft palate, and hypocalcemia, along with microdeletion at chromosome 22. This study is to report twelve Korean patients with CATCH-22 syndrome diagnosed by the fluorescent in situ hybridization (FISH) method. METHOD: Clinical features were analyzed according to the FISH result and the Southern blot analysis using new probes DGCR680 and pDH-1 was performed to correlate with the clinical findings and FISH results. Twelve patients were studied by FISH method and eight of them were studied by Southern blot analysis. RESULTS: Seven patients had typical facial features for CATCH-22 syndrome, but five patients had equivocal face, although they were originally suspected to have the conotruncal face. The main cardiac lesion of eight patients were tetralogy of Fallot (TOF) and seven of them had pulmonary atresia. Two cases had other anomalies in the ventricular outflow tract, being common arterial trunk or pulmonary stenosis. Two cases had a patent arterial duct or atrial septal defect (ASD). All of twelve patients had positive result on FISH study. Among eight patients with positive FISH study, six cases were positive for Southern blot analysis. CONCLUSION: We conclude that CATCH-22 syndrome has variable facial, cardiac and genetic features, and the combined use of probes is recommended for a more accurate diagnosis.