Table 2.
Target gene | ApoE−/− female | DKO female | ApoE−/− male | DKO male |
---|---|---|---|---|
IL-6 | 1.00±0.45 | 1.37±0.80 | 1.00±0.44 | 0.08±0.04 |
IL-18 | 1.00±0.60 | 0.87±0.44 | 1.00±0.34 | 1.269±0.23 |
TNFα | 1.00±0.64 | 0.18±0.13 | 1.00±0.60 | 0.30±0.06 |
ICAM1 | 1.00±0.25 | 0.28±0.18 | 1.00±0.23 | 0.15±0.04* |
VCAM1 | 1.00±0.26 | 0.29±0.15 | 1.00±0.23 | 0.57±0.27 |
MCP1 | 1.00±0.25 | 0.99±0.72 | 1.00±0.05 | 0.73±0.33 |
CXCL1 | 1.00±0.09 | 0.32±0.17* | 1.00±0.33 | 0.20±0.07* |
AT1A | 1.00±0.32 | 0.85±0.47 | 1.00±0.69 | 0.23±0.07 |
AT2 | 1.00±0.13 | 0.33±0.24 | 1.00±0.88 | 0.42±0.15 |
MMP2 | 1.00±0.33 | 0.64±0.40 | 1.00±0.42 | 0.31±0.12 |
MMP9 | 1.00±0.14 | 5.84±2.90 | 1.00±0.33 | 2.00±1.47 |
MMP14 | 1.00±0.53 | 0.52±0.38 | 1.00±0.33 | 0.66±0.16 |
TIMP1 | 1.00±0.11 | 0.53±0.57 | 1.00±0.10 | 0.40±0.07* |
TRAF3IP2 | 1.00±0.34 | - | 1.00±0.23 | - |
RECK | 1.00±0.40 | 0.73±0.31 | 1.00±0.13 | 0.25±0.05* |
ADAM10 | 1.00±0.82 | 7.40±5.20 | 1.00±0.053 | 1.00±0.25 |
ADAM17 | 1.00±0.25 | 0.57±0.37 | 1.00±0.06 | 0.23±0.04* |
IL-6, interleukin-6; IL-18, interleukin-18; TNFα, tumor necrosis factor α; ICAM1, intercellular adhesion molecule 1; VCAM1, vascular cell adhesion molecule; AT1A, angiotensin II receptor, type 1a; AT2, angiotensin II receptor, type 2; MMP, matrix metalloproteinase; TIMP1, tissue inhibitor of matrix metalloproteinase 1; TRAF3IP2, TRAF3-Interacting Protein 2; RECK, reversion-inducing cysteine-rich protein with kazal motifs; ADAM, a disintegrin and metalloproteinase. 18S rRNA served as the endogenous invariant control, and relative gene expression in ApoE−/− female mice were taken as ‘1’. DKO; double knockout mice (TRAF3IP2−/−/ApoE−/−). Values are mean ± SEM (n = 3–5).
indicates significance at p<0.05 when compared between ApoE−/− and DKO mice belonging to the same gender. Statistical significance was calculated by Student’s t-test.