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. Author manuscript; available in PMC: 2017 Jul 4.
Published in final edited form as: Sci Transl Med. 2017 Jan 4;9(371):eaaf8611. doi: 10.1126/scitranslmed.aaf8611

Fig. 2. Transcriptional response of chronic VLUs to BLCC treatment or compression therapy.

Fig. 2

(A) Venn diagram of significantly regulated probes and corresponding genes in BLCC and Control-treated VLUs (fold change >1.5; paired t-test P<0.05). (B) Gene ontology analysis of enriched biological processes among the BLCC-modulated genes. Using Broad Institute GSEA Algorithm, significantly overrepresented functions are grouped by category and listed with enrichment P values (left column) as well as number of corresponding BLCC-influenced genes (parentheses). (C) Ingenuity Pathway Analysis (IPA) of BLCC-modulated genes. The top 10 pathways are shown with corresponding Benjamini-Hochberg-corrected enrichment P values; dotted lines represent genes that are common to the linked pathways. See also table S4. (D) IPA-predicted mechanistic network for BLCC stimulation of immune cell chemotaxis via IL1β; fold changes in IL1β target gene expression after BLCC treatment are shown. (E) Growth factors with IPA-predicted active downstream signaling in response to BLCC treatment, as indicated by overlap of their known targets with BLCC-modulated genes (Fisher’s exact test, P<0.05) as well as by activation (Z) score > 2 reflecting consistent gene expression changes in response to BLCC treatment (11). TGFB1= transforming growth factor beta 1; HGF=hepatocyte growth factor; VEGFA= vascular endothelial growth factor; PDGF=platelet-derived growth factor. See also fig. S2 and table S5.