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. 2013 Nov;347(2):288–297. doi: 10.1124/jpet.113.207316

Fig. 1.

Fig. 1.

MCPIP participates in MCP-1-induced transdifferentiation of BMNCs into ECs. BMNCs were plated in EBM medium on six-well plate coated with fibronectin and treated with MCP-1 in the absence or presence of siRNA against MCPIP for 48 hours. (A) Expression of monocytic cell marker CD11b and EC marker Tie-2 was evaluated by RT-PCR. β-actin served as internal control. (B) Relative mRNA expression of cell surface markers is presented in bar graphics. *P < 0.01 versus untreated control or in the presence of MCPIP siRNA. (C) Representative photomicrographs after 3 days in culture show numbers of cells displaying cobblestone-like morphology in MCP-1-treated BMNCs and siRNA against MCPIP inhibited MCP-1-induced morphology changes in BMNCs. (D) Representative photomicrographs after 3 days in culture show numbers of cells uptaking DiI-acLDL in MCP-1-treated BMCs and siRNA against MCPIP inhibited DiI-acLDL uptake by MCP-1-treated BMNCs. Cells uptaking DiI-acLDL were observed under a phase-contrast/fluorescent microscopy. The red fluorescence indicates intracellular DiI-acLDL.