{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T23:01:09Z","timestamp":1791846069559,"version":"4.3.4"},"reference-count":61,"publisher":"American Physiological Society","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Physiological Genomics"],"published-print":{"date-parts":[[2012,6,1]]},"abstract":"<jats:p>Genomic studies on fetal alcohol spectrum disorders (FASD) have utilized either genome-wide microarrays\/bioinformatics or targeted real-time PCR (RT-PCR). We utilized herein for the first time a novel digital approach with high throughput as well as the capability to focus on one physiological system. The aim of the present study was to investigate alcohol-induced alterations in uterine angiogenesis-related mRNA abundance using digital mRNA technology. Four biological and three technical replicates of uterine arterial endothelial cells from third-trimester ewes were fluorescence-activated cell sorted, validated, and treated without or with binge-like alcohol. A capture probe covalently bound to an oligonucleotide containing biotin and a color-coded reporter probe were designed for 85 angiogenesis-related genes and analyzed with the Nanostring nCounter system. Twenty genes were downregulated (\u2193) and two upregulated (\u2191), including angiogenic growth factors\/receptors (\u2193placental growth factor), adhesion molecules (\u2193angiopoietin-like-3; \u2193collagen-18A1; \u2193endoglin), proteases\/matrix proteins\/inhibitors (\u2193alanyl aminopeptidase; \u2193collagen-4A3; \u2193heparanase; \u2193plasminogen, \u2191plasminogen activator urokinase; \u2193platelet factor-4; \u2193plexin domain containing-1; \u2193tissue inhibitor of metalloproteinases-3), transcription\/signaling molecules (\u2193heart and neural crest derivatives-2; \u2193DNA-binding protein inhibitor; \u2193NOTCH-4; \u2193ribosomal protein-L13a1; \u2193ribosomal protein large-P1), cytokines\/chemokines (\u2193interleukin-1B), and miscellaneous growth factors (\u2193leptin; \u2193platelet-derived growth factor-\u03b1); \u2193transforming growth factor (TGF-\u03b1; \u2191TGF-\u03b2 receptor-1). These novel data show significant detrimental alcohol effects on genes controlling angiogenesis supporting a mechanistic role for abnormal uteroplacental vascular development in FASD. The tripartite digital gene expression system is therefore a valuable tool to answer many additional questions about FASD from both mechanistic as well as ameliorative perspectives.<\/jats:p>","DOI":"10.1152\/physiolgenomics.00009.2012","type":"journal-article","created":{"date-parts":[[2012,4,26]],"date-time":"2012-04-26T00:14:24Z","timestamp":1335399264000},"page":"622-628","source":"Crossref","is-referenced-by-count":15,"title":["Multiplexed digital quantification of binge-like alcohol-mediated alterations in maternal uterine angiogenic mRNA transcriptome"],"prefix":"10.1152","volume":"44","author":[{"given":"Jayanth","family":"Ramadoss","sequence":"first","affiliation":[{"name":"Obstetrics and Gynecology, University of Texas Medical Branch, Galveston, Texas; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ronald R.","family":"Magness","sequence":"additional","affiliation":[{"name":"Perinatal Research Laboratories, Department of Obstetrics and Gynecology, and 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