کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10933903 | 1093870 | 2005 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Cyclooxygenase-1 signaling is required for vascular tube formation during development
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کلمات کلیدی
COXTubulogenesisPGF2αPGE2cyclooxygenase - آنزیم سیکلواکسیژنازAngiogenesis - آنژیوژنزIndomethacin - اندومتاسینnephric duct - مجرای نافریwild-type - نوع وحشیindo - هندوProstaglandin E2 - پروستاگلاندین E2Prostaglandin E2 (PGE2) - پروستاگلاندین E2 (PGE2)Prostaglandin F2α - پروستاگلاندین F2αProstaglandin endoperoxide synthase - پروستاگلاندین اندپورکسید سنتازprostaglandin - پروستاگلاندینهاKidney - کلیهZebrafish - گورخرماهی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Cyclooxygenase-1 signaling is required for vascular tube formation during development Cyclooxygenase-1 signaling is required for vascular tube formation during development](/preview/png/10933903.png)
چکیده انگلیسی
Prostaglandin endoperoxide synthases (PTGS), commonly referred to as cyclooxygenases (COX-1 and COX-2), catalyze the key step in the synthesis of biologically active prostaglandins (PGs), the conversion of arachidonic acid (AA) into prostaglandin H2 (PGH2). Although COX and prostaglandins have been implicated in a wide variety of physiologic processes, an evaluation of the role of prostaglandins in early mammalian development has been difficult due to the maternal contribution of prostaglandins from the uterus: COX null mouse embryos develop normally during embryogenesis. Here, we verify that inhibition of COX-1 results in zebrafish gastrulation arrest and shows that COX-1 expression becomes restricted to the posterior mesoderm during somitogenesis and to posterior mesoderm organs at pharyngula stage. Inhibition of COX-1 signaling after gastrulation results in defective vascular tube formation and shortened intersomitic vessels in the posterior body region. These defects are rescued completely by PGE2 treatment or, to a lesser extent, by PGF2α, but not by other prostaglandins, such as PGI2, TxB2, or PGD2. Functional knockdown of COX-1 using antisense morpholino oligonucleotide translation interference also results in posterior vessel defect in addition to enlarged posterior nephric duct, phenocopying the defects caused by inhibition of COX-1 activity. Together, we provide the first evidence that COX-1 signaling is required for development of posterior mesoderm organs, specifically in the vascular tube formation and posterior nephric duct development.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Developmental Biology - Volume 282, Issue 1, 1 June 2005, Pages 274-283
Journal: Developmental Biology - Volume 282, Issue 1, 1 June 2005, Pages 274-283
نویسندگان
Yong I. Cha, Seok-Hyung Kim, Lilianna Solnica-Krezel, Raymond N. DuBois,