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Expression and Cellular Localization of 15-Hydroxy-Prostaglandin-Dehydrogenase in Abdominal Aortic Aneurysm
PGE(2) has been implicated in abdominal aortic aneurysm (AAA) associated hypervascularization. PGE(2)-metabolism involves 15-hydroxyprostaglandin-dehydrogenase (15-PGDH) the expression of which in AAA is unknown. The aim of this study was to examine the expression and cell distribution of 15-PGDH in...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4545606/ https://www.ncbi.nlm.nih.gov/pubmed/26287481 http://dx.doi.org/10.1371/journal.pone.0136201 |
Sumario: | PGE(2) has been implicated in abdominal aortic aneurysm (AAA) associated hypervascularization. PGE(2)-metabolism involves 15-hydroxyprostaglandin-dehydrogenase (15-PGDH) the expression of which in AAA is unknown. The aim of this study was to examine the expression and cell distribution of 15-PGDH in AAA. Here, we show that 15-PGDH mRNA levels were significantly higher in aorta samples from patients undergoing AAA repair than in those from healthy multiorgan donors. Consequently, the ratio of metabolized PGE(2) secreted by aortic samples was significantly higher in AAA. AAA production of total PGE(2) and PGE(2) metabolites correlated positively with PGI(2) production, while the percentage of metabolized PGE(2) correlated negatively with the total amount of PGE(2) and with PGI(2). Transcript levels of 15-PGDH were statistically associated with leukocyte markers but did not correlate with microvascular endothelial cell markers. Immunohistochemistry revealed 15-PGDH in the areas of leukocyte infiltration in AAA samples, mainly associated with CD45-positive cells, but not in normal aorta samples. We provide new data concerning 15-PGDH expression in human AAA, showing that 15-PGDH is upregulated in AAA and mainly expressed in infiltrating leukocytes. Our data suggest that microvasculature was not involved in PGE(2) catabolism, reinforcing the potential role of microvasculature derived PGE(2) in AAA-associated hypervascularization. |
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