The expression and significance of IL-6, IFN-γ, SM22α, and MMP-2 in rat model of aortic dissection.

OBJECTIVE To examine the expression of interleukin-6 (IL-6), interferon-γ (IFN-γ), smooth muscle 22α (SM22α), and matrix metalloproteinase-2 (MMP-2) and their possible roles in aortic dissections (AD). MATERIALS AND METHODS Male SD rats (3 weeks) were induced for AD using 0.25% β-aminopropionitrile (BAPN) treatment for 6 weeks and were subsequently divided into the model I (with AD) and model II (no AD). Aorta was separated and observed, while TUNEL staining observed apoptosis of aortic vascular smooth muscle cells. Immunohistochemistry (IHC) staining measured the positive expression of IL-6, IFN-γ and MMP-2 in aorta tissues, followed by Western blotting for protein expressions of IL-6, IFN-γ, SM22α, MMP-2, and signal transduction factors phosphorylated c-Jun N-terminal kinase (p-JNK) and p-c-Jun. RESULTS Under an 80% rate of AD formation in model rats, those with AD had significantly higher aorta diameter and apoptosis of aortic vascular smooth muscle cells compared to those without AD or control rats (p<0.05). Elastic fiber gap of model I group was increased, accompanied with elastin fiber breakage and disarrangement. Model rats had significantly higher IL-6, IFN-γ, MMP-2, p-JNK, and p-c-Jun expression than control ones, and lower SM22α expression. No significant difference has been found for these parameters between model I and model II subgroups (p>0.05). There were significantly positive correlations between IL-6 versus MMP-2, IL-6 versus p-JNK, IFN-γ versus MMP-2, IFN-γ versus p-c-Jun in the model I group (p<0.05). CONCLUSIONS IL-6, IFN-γ, and MMP-2 expressed highly in AD. During AD formation, IL-6 and IFN-γ may enhance MMP-2 expression and increase extracellular matrix degradation of aorta vascular wall via JNK signal pathway. The apoptosis and phenotype transformation of vascular smooth muscle cells is likewise correlated with AD formation.