Tetsufumi Yamamoto

Bone Marrow–Derived Cells Contribute to Vascular Inflammation but Do Not Differentiate Into Smooth Muscle Cell Lineages

Background— It has been proposed that bone marrow–derived cells infiltrate the neointima, where they differentiate into smooth muscle (SM) cells; however, technical limitations have hindered clear identification of the lineages of bone marrow–derived “SM cell–like” cells. Methods and Results— Using a specific antibody against the definitive SM cell lineage marker SM myosin heavy chain (SM-MHC) and mouse lines in which reporter genes were driven by regulatory programs for either SM-MHC or SM &agr;-actin, we demonstrated that although some bone marrow–derived cells express SM &agr;-actin in the wire injury–induced neointima, those cells did not express SM-MHC, even 30 weeks after injury. Likewise, no SM-MHC+ bone marrow–derived cells were found in vascular lesions in apolipoprotein E−/−mice or in a heart transplantation vasculopathy model. Instead, the majority of bone marrow–derived SM &agr;-actin+ cells were also CD115+CD11b+F4/80+Ly-6C+, which is the surface phenotype of inflammatory monocytes. Moreover, adoptively transferred CD11b+Ly-6C+ bone marrow cells expressed SM &agr;-actin in the injured artery. Expression of inflammation-related genes was significantly higher in neointimal subregions rich in bone marrow–derived SM &agr;-actin+ cells than in other regions. Conclusions— It appears that bone marrow–derived SM &agr;-actin+ cells are of monocyte/macrophage lineage and are involved in vascular remodeling. It is very unlikely that these cells acquire the definitive SM cell lineage.

Pulmonary Intimal Sarcoma Treated by a Left Pneumonectomy with Pulmonary Arterioplasty Under Cardiopulmonary Bypass: Report of a Case

Intimal sarcoma of the pulmonary artery is a rare disease. This neoplasm was characterized by an aggressive extension to the lumen of the pulmonary artery, thus mimicking a pulmonary thromboembolism. We herein report a 44-year-old woman who was diagnosed as having primary intimal sarcoma of the left lung preoperatively by transbronchial biopsy. The tumor originated in the pulmonary artery in the left lung, extending to the main pulmonary trunk via the pulmonary arterial lumen, thus resulting in stenosis of the main pulmonary trunk. A complete resection of the tumor with the left pneumonectomy and the pulmonary arterioplasty was successfully performed under cardiopulmonary bypass with vacuum assisted venous drainage.

The angiotensin II type 1 receptor blocker valsartan attenuates graft vasculopathy

AbstractObjectiveTransplant arteriosclerosis remains the major cause of graft failure after cardiac transplantation. Here, we investigated the effects of the angiotensin II type 1 receptor blocker valsartan on the development of transplant arteriosclerosis in a murine model of cardiac transplantation.MethodsHearts from DBA/2 (H–2d) mice were heterotopically transplanted into B10.D2 (H–2d) mice. Recipients were treated with oral administration of valsartan (10 mg/kg/day) or vehicle.ResultsMorphometrical analysis of the cardiac allografts harvested at 30 days revealed that valsartan significantly reduced the development of coronary atherosclerosis (intima/media ratio: 0.39 ± 0.05 vs. 0.66 ± 0.08, P < 0.01). At two weeks after transplantation, there was no significant difference between the two groups in expression of adhesion molecules and cytokines. Valsartan significantly reduced the number of peripheral mononuclear cells that differentiated into smooth muscle–like cells in the presence of basic fibroblast growth factor and platelet–derived growth factor BB (18.0 ± 1.5 vs. 30.3 ± 4.4 cells/HPF, P = 0.01).ConclusionsThese results suggest that angiotensin II plays a role in the pathogenesis of transplant arteriosclerosis and that blockade of angiotensin II type 1 receptor might be effective as a prophylactic therapy for transplant arteriosclerosis along with conventional immunosuppressive drugs.

One-stage Repair of Total Descending Aorta for Extended Pathologies

Objectives: One of the potential solutions for embolic events in aortic surgery is to perform aggressive replacement for extended pathologies. The aim of this review was to assess outcomes for aggressive one-stage repair of total descending aorta.