This study investigated the expression and role of immunoproteasome (i-
proteasome) in a cell model of
Parkinson's disease (PD). The cytotoxicity of
rotenone was measured by
CCK-8 assay. The i-
proteasome β1i subunit PSMB9 was suppressed by a specific
shRNA or transfected with an overexpression plasmid in the SH-SY5Y cells. Under the exposure to
rotenone or not, the expression of constitutive
proteasome β subunits, i-
proteasome βi subunits, antigen presentation related
proteins, α-syn and TH were detected by Western blot in PSMB9-silenced or -overexpressed cells, and the proteasomal activities were detected by fluorogenic
peptide substrates. The location of i-
proteasome βi subunits and α-syn were detected by immunofluorescence staining. The levels of ROS, GSH and MDA were measured by commercial kits. Cell apoptosis was detected by flow cytometry. Besides impairing the constitutive proteasomes,
rotenone induced the expression of βi subunits of i-
proteasome and antigen presentation related
proteins such as TAP1, TAP2 and MHC-I. Silencing or overexpressing PSMB9 had no obvious effect on the levels of other subunits, but could regulate the
chymotrypsin-like activity of
20S proteasome and the expression of TAP1, TAP2 and MHC-I. Three βi subunits (PSMB9, PSMB10, PSMB8) of i-
proteasome were all co-localized with α-syn. PSMB9 knockdown aggravated accumulation of α-syn, degradation of TH, release of ROS, increased level of MDA, decreased level of GSH and eventually promoted apoptosis in SH-SY5Y cells after
rotenone treatment, while over-expression of PSMB9 could attenuate these toxic effects of
rotenone. I-
proteasome is activated in SH-SY5Y cells treated with
rotenone and may play a neuroprotective role.