Figure 4
Inhibition of CCR2 activity blocks MCP-1–induced VSMC migration. (A) MCP-1 receptor CCR2 was expressed in VSMCs and 10T1/2 cells. Total RNAs were isolated for RT-PCR using primers for rabbit and mouse CCR2, respectively, or GAPDH (as control). The data are representative of 3 individual experiments. Negative control (NC) had no cDNA templates. (B) The confluent VSMC monolayers were wounded by scraping and treated with MCP-1 (10 ng/mL) or together with RS-102895 (300 nM) in serum-free medium. DMSO was the solvent of RS-102895. Cell migration to the wound surface was monitored from 0 to 36 hours. A representative was shown (bar represents 200 μm) and the migrated distance of the wound edge quantitated (bottom panel). Asterisks indicate a significant difference of migrated distance compared with the control (*P < .05, **P < .01; n = 3). Error bars indicate SD.

Inhibition of CCR2 activity blocks MCP-1–induced VSMC migration. (A) MCP-1 receptor CCR2 was expressed in VSMCs and 10T1/2 cells. Total RNAs were isolated for RT-PCR using primers for rabbit and mouse CCR2, respectively, or GAPDH (as control). The data are representative of 3 individual experiments. Negative control (NC) had no cDNA templates. (B) The confluent VSMC monolayers were wounded by scraping and treated with MCP-1 (10 ng/mL) or together with RS-102895 (300 nM) in serum-free medium. DMSO was the solvent of RS-102895. Cell migration to the wound surface was monitored from 0 to 36 hours. A representative was shown (bar represents 200 μm) and the migrated distance of the wound edge quantitated (bottom panel). Asterisks indicate a significant difference of migrated distance compared with the control (*P < .05, **P < .01; n = 3). Error bars indicate SD.

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