Epoxomicin, a potent and selective proteasome inhibitor, exhibits in vivo antiinflammatory activity - PubMed (original) (raw)
Epoxomicin, a potent and selective proteasome inhibitor, exhibits in vivo antiinflammatory activity
L Meng et al. Proc Natl Acad Sci U S A. 1999.
Abstract
The proteasome regulates cellular processes as diverse as cell cycle progression and NF-kappaB activation. In this study, we show that the potent antitumor natural product epoxomicin specifically targets the proteasome. Utilizing biotinylated-epoxomicin as a molecular probe, we demonstrate that epoxomicin covalently binds to the LMP7, X, MECL1, and Z catalytic subunits of the proteasome. Enzymatic analyses with purified bovine erythrocyte proteasome reveal that epoxomicin potently inhibits primarily the chymotrypsin-like activity. The trypsin-like and peptidyl-glutamyl peptide hydrolyzing catalytic activities also are inhibited at 100- and 1,000-fold slower rates, respectively. In contrast to peptide aldehyde proteasome inhibitors, epoxomicin does not inhibit nonproteasomal proteases such trypsin, chymotrypsin, papain, calpain, and cathepsin B at concentrations of up to 50 microM. In addition, epoxomicin is a more potent inhibitor of the chymotrypsin-like activity than lactacystin and the peptide vinyl sulfone NLVS. Epoxomicin also effectively inhibits NF-kappaB activation in vitro and potently blocks in vivo inflammation in the murine ear edema assay. These results thus define epoxomicin as a novel proteasome inhibitor that likely will prove useful in exploring the role of the proteasome in various in vivo and in vitro systems.
Figures
Figure 1
Structure of epoxomicin.
Figure 2
Epoxomicin biotin binds four proteasome catalytic subunits. EL4 murine thymoma cells (3 × 105) were incubated with 5 μM epoxomicin-biotin without (lane 1) and with (lane 2) 50 μM epoxomicin pretreatment. Human B cell lymphoma cells LCL 721.45 (lane 3) and LCL 721.174 (lane 4) were labeled with 5 μM epoxomicin-biotin. Biotinylated proteins were visualized by using avidin-horseradish peroxidase and chemiluminescence.
Figure 3
Accumulation of p53 (A) and ubiquitinated proteins (B) in epoxomicin-treated cells. (A) α-p53 immunoblot analyses of HUVECs treated with 100 nM epoxomicin (Epx), 5 μM lactacystin (Lac), or vehicle (ctrl) for 6 hr. (B) α-Ubiquitin immunoblot analyses of HeLa cells treated with 10 μM epoxomicin or peptide inhibitor Z-LLL-H for 2 hr.
Figure 4
Epoxomicin inhibits activation of NF-κB. (A) IκBα degradation induced by TNF-α is prevented by epoxomicin. HeLa cells were treated with epoxomicin (10 μM) or Z-LLL-H (10 μM) for 2 hr and subsequently treated with TNF-α (10 ng/ml) for 15 min. Western blot analysis of cell lysates was performed to measure IκBα levels as in Fig. 3. (B) EMSA analysis of NF-κB DNA-binding activity. HeLa cells were treated with increasing concentrations of epoxomicin for 2 hr, and, subsequently, 10 ng/ml TNF-α was added to drug-treated cells or to untreated cultures and incubated for 1 hr. Equal amounts of protein from nuclear extracts prepared from untreated and treated cultures were incubated with a radiolabeled NF-κB oligonucleotide or a control AP-2 oligonucleotide and fractionated on 4% polyacrylamide gels. Dried gels were exposed to a PhosphorImaging screen. The amount of radioactivity in the transcription factor-retarded bands was quantitated and represented as fold-change of treated over that of untreated samples. Shown are TNF-α alone (lanes 1 and 5) and TNF-α plus epoxomicin (100 nM, lanes 2 and 6; 1 μM, lanes 3 and 7; and 10 μM, lanes 4 and 8).
Figure 5
Epoxomicin inhibits inflammation in vivo. (A) CS to picrylchloride. BALB/c mice were immunized with picrylchloride by topical application to shaved chest and abdomen. One group of immunized mice (n = 4) was treated with epoxomicin daily from the time of immunization until the time of ear challenge, whereas the control immunized group (n = 4) was treated with vehicle. On day 6 postimmunization, all mice were skin-challenged by painting both ears with 0.8% picrylchloride. Ear swelling responses were measured before (0 hr) and 24 hr after ear challenge. (B) Irritant sensitivity (IS) response to picrylchloride. Nonimmunized BALB/c mice were injected with epoxomicin (n = 4) or vehicle (n = 4) before ear challenge with 0.8% picrylchloride, and ear swelling measurements were made 0 and 24 hr post-ear challenge. Results in CS and IS assays are expressed as 24-hr measurement minus 0-hr measurement.
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