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. 2004 Mar;135(3):497–504. doi: 10.1111/j.1365-2249.2004.02401.x

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© 2004 Blackwell Publishing Ltd

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Fig. 5 — Antibodies to BP180 induced both elevated tPA protein and mRNA levels in cultured normal human epidermal keratinocytes (NHEK). Cultured NHEK were treated for a 9 h incubation time with 4 and 8 mg/ml IgG from rabbit R594 (immunized against recombinant human BP180 NC16A; □), with preimmune rabbit IgG (), and with medium alone (▪). (a) Culture supernatants were assayed for tPA and uPA reactivity in quadruplicate by ELISA. Bars indicate mean ± SD (ng/ml). (b) tPA mRNA was detected by RT-PCR and expressed as ratio to GAPDH. Asterisks indicate statistical significant difference between R594 IgG- and preimmune IgG-treated cells (*P < 0·05, ***P < 0·001). This pattern is representative of the pattern seen in 2 separate experiments with keratinocytes from different donors.

Inline graphic — Antibodies to BP180 induced both elevated tPA protein and mRNA levels in cultured normal human epidermal keratinocytes (NHEK). Cultured NHEK were treated for a 9 h incubation time with 4 and 8 mg/ml IgG from rabbit R594 (immunized against recombinant human BP180 NC16A; □), with preimmune rabbit IgG (), and with medium alone (▪). (a) Culture supernatants were assayed for tPA and uPA reactivity in quadruplicate by ELISA. Bars indicate mean ± SD (ng/ml). (b) tPA mRNA was detected by RT-PCR and expressed as ratio to GAPDH. Asterisks indicate statistical significant difference between R594 IgG- and preimmune IgG-treated cells (*P < 0·05, ***P < 0·001). This pattern is representative of the pattern seen in 2 separate experiments with keratinocytes from different donors.