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DOI 10.1111/j.1365-2559.2008.02979.x

Медицинская библиотека · Histopathology · 2008

Calcitonin receptor immunoreactivity associated with specific cell types in diseased radial and internal mammary arteries.

Wookey P J, Zulli A, Buxton B F, Hare D L

СтатьяПоддержка исследования: вне правительства СШАПеревод в очереди

Аннотация

AIMS: To determine and quantify calcitonin receptor (CTR) immunoreactivity associated with specific cell types within, and associated with, the endothelial layers, neo-intima, media and vasa vasorum of diseased radial and internal mammary arteries.

METHODS AND

RESULTS

Immunohistochemistry and anti-CTR antibodies were used to identify positive cells within remnants of diseased human radial (n = 3) and internal mammary arteries (n = 4) that remained after bypass surgery. Three cell types expressed CTR, including endothelial cells, fibroblast-like cells within the neo-intima, and cellular structures aligned with the smooth muscle cells of the media. Other smaller cells within the surrounding parenchyma of the vasa vasorum of diseased vessels and blood-borne cells were also immunoreactive. Immunoquantification of CTR expression (Intensity x Proportional Area) in the endothelium (P < 0.05), neo-intima (P < 0.02) and media (P < 0.03) established a significant statistical correlation (Students' two-tailed t-test) with the ratio of intimal/media thickness.

CONCLUSIONS

Increased immunoreactivity developed using anti-CTR antibodies was associated with specific cell types in the endothelial layers, neo-intima, media and vasa vasorum of diseased regions of radial and internal mammary arteries, in which there was an increased intimal/media ratio. Furthermore, CTR+, blood-borne cells present in the vessels of diseased regions suggest recruitment into these surrounding tissues.

Для цитирования: Wookey P J, Zulli A, Buxton B F, Hare D L. Calcitonin receptor immunoreactivity associated with specific cell types in diseased radial and internal mammary arteries.. Histopathology. 2008. DOI: 10.1111/j.1365-2559.2008.02979.x.

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