p38 MAPK- and SAPK/JNK-related pathways contribute to increased tube formation in EPCs under low concentrated oxLDL.

<p>(A) Following treatment of EPCs with 0–50 μg/mL of oxLDL for 4 hours, the phosphorylation of p38 MAPK, SAPK/JNK and ERK1/2 were analyzed by Western blot. The total p38 MAPK, SAPK/JNK, ERK1/2, and β-actin protein levels were used as loading controls. The graph showed the quantitative activation of p38 MAPK (phospho-p38MAPK/total- p38MAPK ratio), SAPK/JNK (phospho-SAPK/JNK/total-SAPK/JNK ratio), and Akt (phospho-ERK1/2/total-ERK1/2 ratio) density in oxLDL-treated EPCs. (B) EPCs were pretreated with SP600125, PD98059, or SB203580 for 1 hour prior to treatment with 5 or 50 μg/mL oxLDL for 24 hours. (C) Treatment of SP600125, PD98059, or SB203580 alone for 24 hours. <i>In vitro</i> angiogenesis was assayed using ECMatrix gel. (D) EPCs were pretreated with SP600125 or SB203580 for 1 hour prior to treatment with 5 μg/mL oxLDL for 24 hours. The NO-containing conditional medium was analyzed using electron spin resonance spectroscopy. Data are expressed as the mean ± SEM of three experiments performed in triplicate. *<i>p</i> < 0.05 was considered significant. (E) EPCs were pretreated with SP600125 or SB203580 for 1 hour prior to treatment with 5 μg/mL oxLDL for 2 hours, subsequently Akt activation (phosphorylation) was analyzed by Western blot. Total Akt protein levels were used as loading controls.