<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE304nnn/GSE304388/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE304388</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Retinoic Acid-Mediated Signaling Regulates Allantoic and Fetoplacental Vascularization</name><description>The placenta is vital for fetal development, and altered placental vascularization underlies prevalent disorders, including fetal growth restriction, prematurity, and pregnancy complications. Impaired placental vascularization is associated with Vitamin A deficiency, but mechanisms are undefined. To investigate this, we used retinoic acid (RA)-deficient Raldh2⁻/⁻ embryos, and found they exhibit placental endothelial hyperproliferation and impaired arterial-venous remodeling, which were rescued by providing all‑trans‑RA (ATRA) via maternal diet. Single cell RNA sequencing of E9.5 Raldh2+/+, Raldh2⁻/⁻,and Raldh2⁻/⁻+ATRA placental cells, and functional assays, revealed that RA regulates endothelial growth and vascular remodeling via Notch signaling.</description><dates><publication>2026/02/17</publication></dates><accession>GSE304388</accession><cross_references><GSM>GSM9149797</GSM><GSM>GSM9149799</GSM><GSM>GSM9149798</GSM><GSM>GSM9149801</GSM><GSM>GSM9149800</GSM><GSM>GSM9149802</GSM><GPL>30172</GPL><GSE>304388</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>