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. Author manuscript; available in PMC: 2021 Nov 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2020 Aug 20;40(11):2632–2648. doi: 10.1161/ATVBAHA.120.314948

Figure 2. Marked ability of the EC-derived factors, PDGF-BB, PDGF-DD and ET-1, to stimulate pericyte motility in 3D matrices and identification of pharmacologic inhibitors that block this response.

Figure 2.

(A, B, and C) Nuclear-GFP labeled pericyte motility was analyzed over the indicated time frames and experimental conditions. These time lapse image stacks were compressed into a single image, so that the “footprints” or “tracks” of pericyte movements can be observed. All cells begin suspended in the 3D collagen gel. (A) Nuclear tracking of pericyte motility over the course of 72 hours. Motility of pericytes when seeded on their own (top row), pericyte motility when co-cultured with ECs (bottom row). (B-G) No additional growth factors = Control; PDGF-BB (20 ng/ml), PDGF-DD (20 ng/ml) and ET-1 (2×10−8 M) = +PDGFs and ET-1; 20 μM CI 1020 (ET-1 receptor A antagonist), 1 μM imatinib (PDGFR inhibitor), 1 μM gefitinib (EGFR inhibitor), 10 μM SB 431542 (ALK5 inhibitor) = +CIGS. (B) Pericytes 0–72 hr compressed time lapse movie, (D) 0–72 hr pericyte motility quantitation, (C) Pericyte 72–120 hr compressed time lapse movie (E) 72–120 hr pericyte motility quantitation. (A-E) Bar equals 200 μm; n≥8. (F) Aggregated pericytes suspended in 3D collagen gel for 24 hr and allowed to invade radially outward. (G) Quantitation of aggregate invasion area. (E-F) Bar equals 100 μm; n≥6. Asterisks indicate significance relative to control at p≤.01.