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. Author manuscript; available in PMC: 2019 Oct 15.
Published in final edited form as: Sci Signal. 2019 Feb 5;12(567):eaan8247. doi: 10.1126/scisignal.aan8247

Figure 4. The CM from hypoxic CAFs silenced for NCBP2-AS2 show a decreased pro-angiogenic activity in vitro and in vivo.

Figure 4

(A, C) Sprouting quantification of ECs treated with CM from hypoxic and normoxic cCAFs (A) or pCAFs (C) transfected with siCTL or siNCBP2-AS2 (2 different siRNAs). N = beads assessed in 3 biological replicates; cCAF Hypoxic CM: siCTL n = 129, siNCBP2-AS2 #1 n = 124 and siNCBP2-AS2 #2 n = 116. Normoxic CM: siCTL n = 121, siNCBP2-AS2 #1 n = 131 and siNCBP2-AS2 #2 n = 122. pCAF Hypoxic CM: siCTL n= 119, siNCBP2-AS2 #1 = 107 and siNCBP2-AS2 #2 = 97. Normoxic CM: siCTL n= 111 beads, siNCBP2-AS2 #1 = 127 and siNCBP2-AS2 #2 = 104. (B, D) RT-qPCR showing the remaining mRNA levels of NCBP2-AS2 normalized to TBP in (B) cCAFs and (D) pCAFs used to produce CM. (E) Vascular density quantification, as measured by Meca32+ and Ng2+ staining of the blood vessels (y axis), of subcutaneous sponges which were embedded with CM derived from hypoxic CAFs transfected with siCTL or siNCBP2-AS2. N = ½ sponges derived from 6 mice per group. T-test. (F) RT-qPCR showing the remaining mRNA levels of NCBP2-AS2 normalized to TBP in CAFs producing the CM used in the sponge assay in (E). * p < 0.05, *** p < 0.001, **** p < 0.0001, NS: not significant.