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. Author manuscript; available in PMC: 2014 Mar 1.
Published in final edited form as: Atherosclerosis. 2012 Dec 19;227(1):65–71. doi: 10.1016/j.atherosclerosis.2012.12.003

Fig. 4.

Fig. 4

The N-terminal domain of apoE3 and its isoforms inhibit miR221/miR222 in VSMCs. (A) Serum-starved VSMCs were incubated with 10% FBS for 24 h in the absence (control; C) or presence of 2 μM ApoE3, or the N- and C-terminal fragments of ApoE3. (B) Serum-starved VSMCs were incubated with 10% FBS for 24 h in the absence or presence of 2 μM apoE2, apoE3 or apoE4. Total RNA was isolated, and miR221/222 levels were determined by RT-qPCR. (C) The experiment in B was repeated, but the VSMCs were incubated for 48 h on coverslips. The cells were analyzed for EdU incorporation by immunofluorescence microscopy. For all panels, results are expressed as mean ± SD, n = 3. Significance was determined by 2-tailed t-test as defined in the legend to Fig. 1.