Fig. 7
From: Single-cell transcriptomics reveals common epithelial response patterns in human acute kidney injury
Multi-channel in situ hybridizations confirm the presence of the four “New” cell states in TALs. A In situ hybridizations for oxidative stress-related gene ALDOB (marker gene of TAL-New 1), hypoxia-induced gene SLC2A1 (marker gene of TAL-New 2), and canonical TAL marker gene SLC12A1. Note that the TAL-New 1 abundance is not significantly different between AKI and control samples (compare to Fig. 6B). TAL-New 1 cells based on ALDOB expression are therefore also present in control samples. Moreover, ALDOB is also expressed in PT cells. B Feature plots highlighting the expression of ALDOB and SLC2A1 in TALs (compare to Fig. 6A) as well as box plots showing the expression of the respective genes in TALs in control versus AKI samples. C In situ hybridizations for inflammation response gene SERPINA1 (marker gene of TAL-New 3), EMT-associated gene MET (marker gene of TAL-New 4), and canonical TAL marker gene SLC12A1. Scale bars as indicated. P-value: * < 0.05, ** < 0.01, *** < 0.001. CPM, counts per million