Fig. 2: Anti-sense oligonucleotide inhibition of miR-200b in dermal fibroblasts induces vasculogenic state. | Nature Communications

Fig. 2: Anti-sense oligonucleotide inhibition of miR-200b in dermal fibroblasts induces vasculogenic state.

From: Identification of a physiologic vasculogenic fibroblast state to achieve tissue repair

Fig. 2: Anti-sense oligonucleotide inhibition of miR-200b in dermal fibroblasts induces vasculogenic state.The alternative text for this image may have been generated using AI.

a Quantitative gene expression of key representative transcripts from the cDNA prepared and used for single cell RNA sequencing at day 7 post-miR-200b inhibition. Data are mean ± S.D (n = 5–6). b Immunofluorescence of eNOS expression in HADF transfected with control or miR-200b inhibitor at d7 post in vitro TNT. Scale, 200 µm. Data are mean ± S.D (n = 6–8). c Immunocytochemistry of acLDL uptake in HADF transfected with control or miR-200b inhibitor at d7 post in vitro TNT. Scale, 200 µm. Data are mean ± S.D (n = 8–10). d Representative images showing in vitro Matrigel tube formation by vasculogenic fibroblasts and its analysis. HMEC were used as positive control. Scale, 200 µm. Results represent mean ± S.D (n = 10). e Schematic diagram showing the experimental design for in vivo collagen gel assay. f Immunofluorescence confocal image of in vivo collagen gel assay showing lectin perfused vessels of HADF origin treated with miR 200b inhibitor at day 28. Such perfused vessels were absent in control groups where HADF were treated with only control inhibitor. Scale, 50 µm. Data in a–c were analyzed by two-tailed unpaired Student’s t test. Data in d was analyzed by one-way analysis of variance with the post-hoc Bonferroni multiple comparison test. Fig 2e created with BioRender.com.

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