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Biomedical subjects

F Numano

Publications and source records attributed to F Numano.

257 records · Page 15Linked to original sources
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Faulty induction of blood-brain barrier functions by astrocytes isolated from stroke-prone spontaneously hypertensive rats.

1. It has been suggested that astrocytes prompt the induction of blood-brain barrier (BBB) functions in cerebrovascular endothelial cells. 2. In the present study we have tried to elucidate the genetic differences between astrocytes isolated from Wistar-Kyoto (WKY) control rats and astrocytes isolated from stroke-prone spontaneously hypertensive rats (SHRSP). 3. We show that endothelial cells develop tight junction-like structures, a reduction in vesicular transport and high electrical resistance when they are co-cultured with astrocytes isolated from WKY rats. In contrast, SHRSP astrocytes have less of an ability to induce BBB functions than do WKY astrocytes. 4. In addition, we demonstrate that SHRSP astrocytes produce enormous quantities of lactic acid when cerebral ischaemia develops. The decrease in pH causes astrocyte swelling and damages BBB functions. 5. Consequently, we reason that genetically weak functions in astrocytes cause disruptions of BBB function and result in widespread cerebral lesions in SHRSP.

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Astrocyte-conditioned medium induces blood-brain barrier properties in endothelial cells.

1. We evaluated the induction of endothelial barrier functions by the type 1 astrocyte-derived supernatant in culture using horseradish peroxidase (HRP) as a parameter. 2. A gel filtration fraction (molecular weight 16-20 kDa) of type 1 astrocyte-derived supernatant reduced plasmalemmal vesicles and induced tight junctions in endothelial cells. 3. In addition, this fraction promoted the uptake of [3H]-glucosamine by endothelial cells. This cell activity disappeared after heating at 95 degrees C for 10 min and was sensitive to trypsin. 4. These results suggest that a type 1 astrocyte-derived protein factor(s) promotes proteoglycan synthesis with a resultant increase in charge selectivity in endothelial cells and plays an important role in the induction of blood-brain barrier functions.

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Role of smooth-muscle cells and macrophages in cardiac allograft arteriosclerosis in rabbits.

Accelerated coronary arteriosclerosis is one of the major complications in allogeneic cardiac transplantation, despite the significant improvement in immunosuppressive therapy. In this study we sought to clarify the cellular components in cardiac allograft arteriosclerotic lesions with monoclonal antibodies specific to either the muscle cell (HHF-35) or the macrophage (RAM-11). Four kinds of heterotopic transplantations were performed in the rabbit: (1) low cholesterol-fed (n = 5), (2) 1% cholesterol-fed (n = 5), (3) low cholesterol-fed and immunosuppressed (n = 6), and (4) 1% cholesterol-fed and immunosuppressed (n = 6). The donor hearts were removed after cardiac arrest in groups 1 and 2, and at 5 weeks after transplantation in groups 3 and 4. In groups 1 and 2 acute rejection was associated with slightly thickened intimal lesions composed of abundant infiltrating mononuclear cells and sparsely intermingled smooth-muscle cells. In group 3 the arterial intima were moderately thickened with the predominant proliferation of smooth-muscle cells. In group 4 coronary lumina were almost completely occupied with the intimal foam cells, which were derived mostly from macrophages and some from smooth-muscle cells. These data suggest that the proliferation of smooth-muscle cells might be a major factor contributing to arteriosclerosis in chronic cardiac rejection and that long-term exposure to hypercholesterolemia could induce the accumulation of smooth-muscle cells or macrophage-derived foam cells.

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