Fig. 2.
Fig. 2. Northern blot and semiquantitative PCR analysis of PAI-2 expression. / (A) Elutriation-purified monocytes from patients with isolated Lp(a) hyperlipidemia (P1, P2), healthy controls with elevated Lp(a) (L1, L2), and 6 controls with low Lp(a) (C1 to C6) were incubated in 20% autologous serum for 18 hours. RNA was isolated and 10 μg total RNA was used to investigate the expression of PAI-2. The film was exposed for 4 hours at −80°C to emphasize the difference in PAI-2 expression in the first 3 lanes. The blot was stripped and hybridized with a GAPDH probe. (B) RNA was prepared from monocytes of patients with isolated Lp(a) hyperlipidemia (P1, P3), healthy probands with elevated Lp(a) (L3, L4), and controls with low Lp(a) (C1, C2, C7, C8, C9, C10, C11, C12) as described in “Materials and methods.” The 100 ng RNA was used to amplify PAI-2 cDNA (20 cycles) or GAPDH cDNA (18 cycles).

Northern blot and semiquantitative PCR analysis of PAI-2 expression.

(A) Elutriation-purified monocytes from patients with isolated Lp(a) hyperlipidemia (P1, P2), healthy controls with elevated Lp(a) (L1, L2), and 6 controls with low Lp(a) (C1 to C6) were incubated in 20% autologous serum for 18 hours. RNA was isolated and 10 μg total RNA was used to investigate the expression of PAI-2. The film was exposed for 4 hours at −80°C to emphasize the difference in PAI-2 expression in the first 3 lanes. The blot was stripped and hybridized with a GAPDH probe. (B) RNA was prepared from monocytes of patients with isolated Lp(a) hyperlipidemia (P1, P3), healthy probands with elevated Lp(a) (L3, L4), and controls with low Lp(a) (C1, C2, C7, C8, C9, C10, C11, C12) as described in “Materials and methods.” The 100 ng RNA was used to amplify PAI-2 cDNA (20 cycles) or GAPDH cDNA (18 cycles).

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