Perivascular adipose tissue exhibits characteristics of active local inflammation, which contributes to the development of atherosclerotic disease as a complication of obesity/metabolic syndrome. However, the precise role of perivascular adipose tissue in the progression of abdominal aortic aneurysm remains unclear. To test the hypothesis that genetic deletion of angiotensin II type 1a (AT) receptor in perivascular visceral adipose tissue (VAT) can attenuate aortic aneurysm formation in apolipoprotein E-deficient (ApoE) mice, we performed adipose tissue transplantation experiments by using an angiotensin II-induced aneurysm murine model, in which we transplanted VAT from ApoE or ApoE AT donor mice onto the abdominal aorta of ApoE recipient mice. Compared with ApoE VAT transplantation, ApoE AT VAT transplantation markedly attenuated aortic aneurysm formation, macrophage infiltration, and gelatinolytic activity in the abdominal aorta. AT receptor activation led to the polarization of macrophages in perivascular VAT toward the proinflammatory phenotype. Moreover, osteopontin expression and gelatinolytic activity were considerably lower in ApoE AT perivascular VAT than in ApoE perivascular VAT, and angiotensin II-induced osteopontin secretion from adipocytes was eliminated after deletion of AT receptor in adipocytes. Notably, induction of macrophage migration by conditioned medium from angiotensin II-stimulated wild-type adipocytes was suppressed by treatment with an osteopontin-neutralizing antibody, and ApoE OPN VAT transplantation more potently attenuated aortic aneurysm formation than ApoE VAT transplantation. Our findings indicate a previously unrecognized effect of AT receptor in perivascular VAT on the pathogenesis of abdominal aortic aneurysm.
Calcification of bioprosthetic valves (BVs) implanted in aortic position can result in gradual deterioration and necessitate aortic valve replacement. The molecular mechanism of calcium deposition on BV leaflets has been investigated, but remains to be fully elucidated. The present study aimed to identify explanted bioprosthetic valve (eBV)-specific proteins using a proteomics approach and to unveil their biochemical and histological involvements in calcium deposition on BV leaflets. Calcification, fibrosis, and glycosylation of the valves were histologically assessed using Von Kossa, Masson's Trichrome and Alcian Blue staining, as well as immunostaining. Protein expression in the explanted biological valves was analysed using proteomics and western blotting. In a histological evaluation, αSMA-positive myofibroblasts were not observed in eBV, whereas severe fibrosis occurred around calcified areas. SDS-PAGE revealed three major bands with considerably increased intensity in BV leaflets that were identified as plasminogen and fibrinogen gamma chain (100 kDa), and fibrinogen beta chain (50 and 37 kDa) by mass analysis. Immunohistochemistry showed that fibrinogen β-chain was distributed throughout the valve tissue. On the contrary, plasminogen was strongly stained in CD68-positive macrophages, as evidenced by immunofluorescence. The results suggest that two important blood coagulation-related proteins, plasminogen and fibrinogen, might affect the progression of BV degeneration.
Summary. This paper deals with changes in intralobular microvascular density and architecture of the rat mammary gland during the reproductive cycle.Morphometrical analysis of india ink-perfused histological sections showed that the vascular density (the percentage of the total area of the vascular lumen to the whole lobular area), was consistently low before pregnancy and slightly increased by the 5th day of gestation. The vascular density increased twofold from the 5th to 10th days and decreased gradually thereafter. This substantial increase may presumably be associated with rapid glandular development, and the subsequent decrease may reflect the hypertrophy of individual acini.Scanning electron microscopy of corrosion casts showed that blood vessels were sparse before the 5th day of gestation and proliferated by capillary sprouts and globular outgrowths of venules by the 18th day. After the 12th day, the blood vessels were organized into round lumps which appeared to correspond in size to individual lobules. By the 18th day, the vessels were remodeled into highly ordered basket like units which disintegrated by the 20th day. The findings suggest that homogenious acini, formed temporally, eventually undergo uneven growth.
We examined the microvasculature of the 7,12-dimethylbenz(a)anthracene (DMBA)-induced rat mammary tumour by scanning electron microscopy of corrosion casts. An elaborate vascular envelope predominantly consisting of sinusoidal and venular vessels was formed around each tumour nodule. These vessels exhibited various abnormal features, whereas arterioles appeared normal. The abnormal vessels possessed many globular outpouches, possibly representing the site of angiogenesis. An additional capillary layer was seen in the marginal boundary between the tumour and host tissue. The lack of centrifugally extruding vessels in this layer may indicate a poor potency for vascular spread of tumour cells into the adjacent normal tissue. Loop-like or glomerular ingrowths were frequently found on the inner aspect of the vascular capsule, which eventually developed into a dense intranodular plexus. Intranodular vessels often showed focal narrowing, tapering and/or rupturing, possibly due to increased tissue pressure caused by proliferating tumour cells. Those surrounding necrotic portions were extremely dilated with occasional periodic varicosities. The features may be associated with the lessening of the tissue pressure resulting from tumour cell collapse.
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