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. 2022 May 19;13:2785. doi: 10.1038/s41467-022-30466-6

Fig. 6. COL1A2 is necessary and sufficient for NF1-deficient Schwann cell growth in vitro.

Fig. 6

A Immunofluorescent staining and corresponding quantitation of Ki67+ human shNF1 Schwann cells (left) and Nf1−/− mouse DRG–NSCs (right) following incubation with hiPSC-sensory neuron conditioned media (CM), with (h P = 0.0007; m P < 0.0001) and without (P < 0.0001) collagenase (n = 6 for all groups), COL1A2 alone with (h P = 0.0036; m P < 0.0001) and without (P < 0.0001) collagenase (n = 6 for all groups), as well as with and without control or short hairpins against COL1A2 (n = 3 for all groups, P < 0.0001) or Col1a2 (vehicle n = 4, control short hairpin n = 7, shCol1a2-1 n = 4, sh Col1a2-2 n = 4, sh Col1a2-3 n = 3, P < 0.0001). B–C (B) Human and (C) mouse cutaneous (cNF) and plexiform neurofibromas (pNF) express COL1A2. Normal brain, lymph node and normal sural (human) or normal sciatic (mouse) nerves were negative for COL1A2 expression. Neurofilament was used as positive control for normal mouse nerve tissue. These data derive from a single-tissue microarray. D COL1A2 RNA expression is increased in human shNF1 Schwann cells (left; P = 0.0014) and mouse Nf1−/− DRG–NSCs (right; P = 0.0012) following COL1A2 treatment. n = 3 for all groups. E COL1A2 RNA expression is increased in human Schwann cells isolated from human cNF (P = 0.0039) and pNF tumors (P = 0.0022) relative to controls. Normal n = 10, cNF n = 11, pNF n = 11. Data are presented as the mean ± SEM. A, E One-way ANOVA with (A) Tukey’s or (E) Dunnett’s multiple comparisons test, or (D) paired two-tailed Student t test. Scale bars, 50 µm. Source data are provided as a Source Data file.