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. 2020 Dec 15;11(5):1261–1273. doi: 10.1016/j.apsb.2020.12.010

Figure 4.

Figure 4

Overexpression of PARP16 results in VSMC proliferation and migration accompany with ER stress. rVSMCs were transfected with lentivirus-mediated Parp16 cDNA (PARP16 OE) or vector (Control) for 72 h, cell lysates were immunoblotted with antibodies against PARP16, p-PERK, p-eIF2α, p-IRE1α, spliced XBP-1, and BIP (A); PCNA, MMP9, cyclin E and cyclin D1 (B); rVSMCs migration ability was tested by wound healing assay, scale bars: 400 μm. (C) and Transwell assay, scale bars: 200 μm (D); rVSMCs proliferation ability was detected by EdU assay, scale bars: 200 μm (E); All data are represented as means ± SEM; ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001 vs. control, each acquired from three individual experiments. (F)–(H) PARP16 selectively ADP-ribosylated PERK and IRE1α during the UPR. hVSMCs with overexpression FLAG-PARP16 were treated PDGF-BB for 36 h, the PARP16 localization was demonstrated by co-immunostaining with calnexin, scale bars: 50 μm. (F); Coimmunoprecipitation using antibody against FLAG in lysates of hVSMCs induced by PDGF (G); Coimmunoprecipitation using anti-ADP-ribose binding reagents in lysates of PDGF-BB-induced hVSMCs (H).