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. Author manuscript; available in PMC: 2010 Mar 2.
Published in final edited form as: Atherosclerosis. 2005 Dec 1;188(2):292–300. doi: 10.1016/j.atherosclerosis.2005.11.002

Figure 7.

Figure 7

Effects of periostin protein secretion on VSMC hapotaxis migration. A. Antibody blockade of periostin reduces VSMC haptotaxis migration. Blockade was achieved by incubation of VSMCs in migration buffer alone (non-Ab) or along with 10 ug/mL of anti-periostin (anti-PN) or rabbit anti-HA antibody (Iso-Ab) in the upper-chamber. Upper-chamber membranes were pre-coated with conditioned medium of quiescent VSMCs that were maintained in the absence (bar 1) or presence of FGF-2 (bars 2, 3, 4). Results are expressed as percentage of the migration observed in the control group (bar 1). *P<0.001 vs bar 1. #P<0.01 vs bar 2 and bar 3.

B. Depletion of secreted periostin protein from VSMC-conditioned medium reduces VSMC haptotaxis migration. Depletion was achieved by immunoadsorption using beads alone (non-Ab) or beads immuno-complexed with indicated concentrations of anti-PN or rabbit anti-HA antibody (Iso-Ab). Upper-chamber membranes were pre-coated with periostin-depleted conditioned-medium obtained in the absence (bar 1) or presence (bars 2 to 5) of FGF-2 treatment. Results are expressed as percentage of the migration observed in the control group (bar 1). *P<0.001 vs bar 1. #P<0.01 vs bar 2 and bar 3.

C. Anti-periostin antibody (anti-PN) does not block vitronectin-induced VSMC haptotaxis migration. Blockade was achieved by incubation of VSMCs in migration buffer containing 10 ug/ml of anti-PN in the upper chambers. Up-chamber membranes were pre-coated with migration buffer alone (control) or containing varying concentrations of vitronectin, or with the conditioned-medium of the FGF-2-treated VSMCs (FGF2-CM).