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. 2012 Oct;47(4):445–453. doi: 10.1165/rcmb.2011-0332OC

Figure 5.

Figure 5.

(A) PLY (30 ng/ml) induces a significant increase in arginase activity within 2 hours in HL-MVECs (n = 6). This effect is blunted upon pretreating the cells for 30 minutes with PKC-α inhibitor Ro32–4032 (10 nM), TIP peptide (27 μM), or the arginase inhibitor (S)-(2-boronoethyl)-l-cysteine (BEC) (100 μM). PLY (30 ng/ml) significantly increases arginase I expression (B) and arginase II expression (C) in HL-MVEsC as assessed by Western blotting. This effect is partially or completely blunted upon pretreating cells with TIP peptide (27 μM) or the PKC-α inhibitor Ro32–4032 (10 nM), respectively (n = 4). (D) The arginase inhibitor BEC (100 μM), upon 1 hour pretreatment, partially blunts PLY (30 ng/ml)-mediated hyperpermeability as assessed by transendothelial resistance in HL-MVECs. Treatment of the cells with the NOS inhibitor l-NAME (100 μM) 1 hour before the BEC treatment abolishes the protective effect of the latter. (E) A 2-hour PLY treatment (30 ng/ml) of HL-MVECs significantly reduces basal NO production in these cells. This PLY effect is prevented upon pretreating the cells 30 minutes before PLY with the PKC-α inhibitor Ro32–4032 (10 nM) or with the TNF-derived TIP peptide (27 μM).