Figure 5. Overexpression of miR-30c prevents injury induced increase of CaMKIIδ and attenuates neointima formation.

Rat carotid artery was balloon injured and locally infected with lentivirus encoding GFP and miR-30c. After 14 days, immunoblotting and histochemistry were employed for protein and morphology analysis. (a) The protein level of CaMKIIδ, calponin, GFP and β-actin was tested in uninjured and injured carotid arteries. Quantified data were normalized over β-actin and shown as mean ± S.E.M., n = 3. *p < 0.05 by paired t-test comparing CaMKIIδ expression between injured (IN) and uninjured (UN) arteries. (b) Injured carotid artery was fixed followed with sectioning (8μm) and staining with hematoxylin and eosin. The areas of medial layer and neointima were measured and quantified. Data shown are the ratio of neointima over medial layer, and presented as mean ± S.E.M., n = 3. ** indicates p < 0.01 by unpaired t-test.