E-MTAB-9703
scRNAseq of femoral artery segments in the context of hind limb ischemia in mice with or without an endothelial cell-specific deletion of transcription factor Prdm16
Femoral artery segments from the ligated ('L') right side (downstream of the ligation site) as well as the corresponding segments from the unligated ('UL') left side were dissected out 3 days after femoral artery ligation in adult mice with or without a long-term (from post-natal day 1 onwards) endothelial-specific deletion of transcription factor Prdm16. Fragments from 4 donor mice were pooled to obtain sufficient cell numbers for sequencing. The experiment existed of 4 samples to be sequenced at single-cell resolution (Prdm16 wild-type L or 'Right_WT'; Prdm16 wild-type UL or 'Left_WT'; Prdm16 endothelial-specific knockout L or 'Right_KO'; Prdm16 endothelial-specific knockout UL or 'Left-KO'). The experiment was intended to identify in situ Prdm16 genotype-dependent genes and corresponding functional pathways in arterial endothelial cells that could be responsible for the observed endothelial dysfunction caused by endothelial-specific Prdm16 deletion in mice upon induction of hind limb ischemia.
Femoral artery segments from the ligated ('L') right side (downstream of the ligation site) as well as the corresponding segments from the unligated ('UL') left side were dissected out 3 days after femoral artery ligation in adult mice with or without a long-term (from post-natal day 1 onwards) endothelial-specific deletion of transcription factor Prdm16. Fragments from 4 donor mice were pooled to obtain sufficient cell numbers for sequencing. The experiment existed of 4 samples to be sequenced at single-cell resolution (Prdm16 wild-type L or 'Right_WT'; Prdm16 wild-type UL or 'Left_WT'; Prdm16 endothelial-specific knockout L or 'Right_KO'; Prdm16 endothelial-specific knockout UL or 'Left-KO'). The experiment was intended to identify in situ Prdm16 genotype-dependent genes and corresponding functional pathways in arterial endothelial cells that could be responsible for the observed endothelial dysfunction caused by endothelial-specific Prdm16 deletion in mice upon induction of hind limb ischemia.