The Uptake of Heparanase into Mast Cells Is Regulated by Its Enzymatic Activity to Degrade Heparan Sulfate.

Mast cells take up extracellular latent heparanase and store it in secretory granules. The present study examined whether the enzymatic activity of heparanase regulates its uptake efficiency. Recombinant mouse heparanase mimicking both the latent and mature forms (L-Hpse and M-Hpse, respectively) was internalized into mastocytoma MST cells, peritoneal cell-derived mast cells, and bone marrow-derived mast cells. The internalized amount of L-Hpse was significantly higher than that of M-Hpse. In MST cells, L-Hpse was continuously internalized for up to 8 h, while the uptake of M-Hpse was saturated after 2 h of incubation. L-Hpse and M-Hpse are similarly bound to the MST cell surface. The expression level of cell surface heparan sulfate was reduced in MST cells incubated with M-Hpse. The internalized amount of M-Hpse into mast cells was significantly increased in the presence of heparastatin (SF4), a small molecule heparanase inhibitor that does not affect the binding of heparanase to immobilized heparin. Enzymatically quiescent M-Hpse was prepared with a point mutation at Glu335. The internalized amount of mutated M-Hpse was significantly higher than that of wild-type M-Hpse but similar to that of wild-type and mutated L-Hpse. These results suggest that the enzymatic activity of heparanase negatively regulates the mast cell-mediated uptake of heparanase, possibly via the downregulation of cell surface heparan sulfate expression.

Surgery for a mitral annulus abscess penetrating into the pericardial cavity.

Although a mitral annulus abscess often develops with infective endocarditis, penetration into the pericardial cavity is a very rare and fatal complication. Herein, we report a case of surgery with thorough debridement and appropriate reconstruction for a mitral annulus abscess with penetration into the pericardial cavity.

Coronary Artery Stenosis Caused by Primary Malignant Pericardial Mesothelioma in a 76-Year-Old Man.

This report describes a 76-year-old man with diabetes mellitus who developed coronary artery stenosis from infiltration of a primary malignant pericardial mesothelioma. Three months before referral to the treating hospital, elevated liver function values and cardiac enzymes led to echocardiography, which revealed a motion abnormality in the anterior wall of the heart. The patient was diagnosed with congestive heart failure and admitted to the hospital, where chest computed tomography showed a tumor above the left atrial appendage that compressed the origin of the left anterior descending artery. He was referred to the treating hospital for surgery. Minimally invasive direct coronary artery bypass grafting was performed, but the mass was not resected because of its infiltrating nature and the potential for medical complications. Histologic examination of a biopsy specimen confirmed a primary malignant pericardial mesothelioma. The bypass procedure resolved the coronary artery stenosis caused by the tumor. Although the optimal treatment for primary malignant pericardial mesothelioma is controversial, minimally invasive methods, such as minimally invasive direct coronary artery bypass grafting, may be used successfully.

Native Valve Attachment to the Prosthetic Valve 2.5 Years After the Third Tricuspid Valve Replacement.

The native tricuspid leaflets are sometimes preserved with tricuspid valve replacement to prevent atrioventricular block or maintain right ventricular function. However, after a tricuspid valve replacement using bioprosthetic valve, a rare complication involving adhesion of the pannus formation to the prosthetic valve may occur. We report the case of a 48-year-old woman who underwent a third tricuspid valve replacement with a bioprosthetic valve for severe tricuspid regurgitation 2.5 years after the redo tricuspid valve replacement.