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Original immunofluorescence images and quantification data supporting PI3K-Akt pathway analysis in microplastic-exposed DSS colitis
Summary
Scientists studying mice with colitis (a form of inflammatory bowel disease) found that exposure to microplastics further activates a specific cell-signaling pathway that's already linked to gut inflammation. This suggests microplastics could potentially make existing gut inflammation worse, though this research was done in mice, not humans, so more work is needed to confirm the same happens in people. This dataset specifically shares the raw images and measurements behind those findings, allowing other researchers to verify the results.
This dataset contains the original immunofluorescence TIFF exports and replicate-level quantification data supporting Figure 9, Supplementary Figure 8, and Supplementary Tables 1–2 of the related manuscript, “Microplastic exposure activates PI3K-Akt signaling in ulcerative colitis: integrated computational toxicology, RNA-seq, GeneMANIA network analysis, and in vivo validation.” The dataset includes p-AKT and p-PI3K staining of mouse colonic tissue from the normal control, DSS-colitis, and DSS-colitis + microplastics groups. For each marker and group, three biologically independent samples are provided. Each sample contains a DAPI image, a red target-channel image, and the corresponding merged image, yielding 54 original TIFF files. All TIFFs are 1920 × 980 pixels and contain 25-µm scale bars. The files were copied and renamed without pixel modification. A manifest links every deposited image to its publication panel, experimental group, biological replicate, fluorescence channel, original source filename, and SHA-256 checksum. Replicate-level Image-Pro Plus measurements and normalized-density values are also included. The p-AKT staining pattern was interpreted as epithelial-predominant based on tissue morphology. Because no epithelial cell-type-specific co-staining was performed, these images do not establish definitive cell-type localization.