Cellular Context of Panx1 Transcript Detection in Experimental Ischemic Stroke

Pannexin 1 (Panx1) participates in ATP release and inflammatory signaling, but its transcript-level distribution after ischemic stroke remains incompletely characterized. We combined a focused bibliometric analysis of 280 publications with reanalysis of GSE174574, comprising three sham and three middle cerebral artery occlusion (MCAO) mouse brain samples collected at 24 h, and a supportive tissue-level comparison using GSE58720, comprising three samples each from sham, MCAO, and MCAO-plus-vascular-endothelial-growth-factor (VEGF) groups. The curated single-cell atlas contained 58,333 cells, of which 640 had detectable Panx1 transcripts. Sample-aware comparisons used equal-weight sample fractions, exact permutation tests, and separately calculated Welch confidence intervals. The MCAO-minus-sham difference in activated microglial detection was 1.153 percentage points (95% confidence interval 0.150–2.155; exact p = 0.10; Benjamini–Hochberg-adjusted p = 0.433). Slingshot described myeloid state-space organization; its primary branch contained 10,492 cells, including 10,487 microglial cells. In bulk tissue, the Panx1 coefficient was −0.311 on the processed-matrix scale (adjusted p = 0.435), whereas an exploratory 16-gene myeloid/inflammatory panel had a higher mean score in MCAO (difference 1.363; exact and adjusted p = 0.10). Removing Panx1 from that panel preserved the direction. The results describe sparse, heterogeneous Panx1 transcript detection and accompanying inflammatory patterns, with limited between-condition inference from three samples per group. They do not establish a Panx1-specific transcriptional program, biological progression, protein induction, or channel activation.