ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR531/001/SRR5314111/SRR5314111_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR531/002/SRR5314112/SRR5314112_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR531/001/SRR5314111/SRR5314111_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR531/002/SRR5314112/SRR5314112_1.fastq.gzprimaryOK200GenomicsDr. Hal Broxmeyer Lab, Microbiology & Immunology, Indiana Universityhttps://www.ebi.ac.uk/ena/browser/view/PRJNA378166Homo sapiensxref:PubMed:29377004PPARγ antagonist GW9662 treatment could enhance ex vivo expansion of human cord blood hematopoietic stem and progenitor cells (HSCs/HPCs). To gain mechanistical insights into how antagonizing PPARγ promotes expansion of HSCs/HPCs, we performed RNA sequencing (RNA seq) analysis to identify genes involved in this process. Loss of function of PPARγ in CB CD34+ cells resulted in downregulation of a number of differentiation associated genes, including CD38, CD1d, HIC1, FAM20C, DUSP4, DHRS3 and ALDH1A2, suggesting that PPARγ antagonist may maintain stemness of CB CD34+ cells, at least in part by preventing differentiation. We also observed that FBP1, encoding fructose 1, 6-bisphosphatase, a negative regulator of glycolytic flux, was significantly downregulated by treating CB CD34+ cells with GW9662. Our study demonstrates that antagonizing PPARγ signaling drives ex vivo expansion of human CB HSCs/HPCs by switching on FBP1 repressed glycolysis and preventing differentiation. Overall design: Total RNA was extracted from Vehicle or GW9662 treated cord blood CD34+ cells, and then RNA sequencing analysis was performed.ENAfalseHomo sapiensRNA sequencing analyisis to identify genes regulated by GW9662 in human cord blood hematopoietic stem and progenitor cells2025-09-242018-03-01PRJNA378166GSE95703960629377004