COX-2 Limits Prostanoid Production in Activated HUVECs and Is a Source of PGH2for Transcellular Metabolism to PGE2by Tumor Cells | Zendy

M. Dolores Salvado | Zendy; Arántzazu Alfranca | Zendy; Amelia Escolano | Zendy; Jesper Z. Haeggström | Zendy; Juan Miguel Redondo | Zendy

Open Access

COX-2 Limits Prostanoid Production in Activated HUVECs and Is a Source of PGH₂for Transcellular Metabolism to PGE₂by Tumor Cells

Author(s) -

M. Dolores Salvado,

Arántzazu Alfranca,

Amelia Escolano,

Jesper Z. Haeggström,

Juan Miguel Redondo

Publication year - 2009

Publication title -

arteriosclerosis thrombosis and vascular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.007

H-Index - 270

eISSN - 1524-4636

pISSN - 1079-5642

DOI - 10.1161/atvbaha.109.188540

Subject(s) - transcellular , prostanoid , prostacyclin , angiogenesis , chemistry , prostaglandin e , endothelial stem cell , prostaglandin , microbiology and biotechnology , thromboxane a2 , downregulation and upregulation , biochemistry , biology , cancer research , receptor , in vitro , gene

Inducible expression of cyclooxygenase-2 (COX-2) and terminal prostaglandin synthases (tPGS) has been mainly analyzed in tumor, stromal, and inflammatory cells, and little is known about the regulation of prostanoid biosynthesis by endothelial cells. Here we characterize the profile of prostanoids produced by activated HUVECs and analyze the expression and activities of tPGS.

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