{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE306nnn/GSE306399/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE306399"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Transcriptomic changes in HUVEC with PDL1 knockdown","description":"Programmed cell death ligand-1 (PD-L1) is an immune checkpoint protein expressed in vascular endothelial cells (ECs). In contrast to cancer, our understanding of endothelial PD-L1 in relation to metabolic syndromes and its vascular complications is less studied. For example, its regulation and intrinsic function remain unclear. Here, we show endothelial PD-L1 is regulated by leptin receptor signaling. In particular, endothelial PD-L1 expression is likely affected by leptin resistance. A lack of leptin receptors leads to PD-L1 downregulation in vascular ECs via post-translational degradation. To understand the fundamental roles of endothelial PD-L1, RNA interference and selective knockout are employed in human endothelium and animals, respectively. Silencing or deleting endothelial PD-L1 expression delays the cycle progression and proliferation, because of Ras/MAPK inactivation. During obesity, endothelial PD-L1 deficiency impairs the EC turnover and worsened the vascular function. Overall, we provide a new insight of how endothelial PD-L1 contributes to vascular homeostasis, suggesting its pathophysiological importance in maintaining cellular turnover.","dates":{"publication":"2026/10/02"},"accession":"GSE306399","cross_references":{"GSM":["GSM9198838","GSM9198837","GSM9198836","GSM9198835","GSM9198834","GSM9198833"],"GPL":["24676"],"GSE":["306399"],"taxon":["Homo sapiens"]}}