Fig. 4: SerpinB7 deficiency promotes proliferation and suppresses differentiation in keratinocytes.

A NHEK cells were transfected with shCT and sh-SerpinB7. The mRNA level of SerpinB7 was measured by RT-PCR. B CaCl₂-induced Filaggrin, Loricrin, and KRT10 expression in shCT and sh-SerpinB7 NHEKs at 0–72 h was measured by RT-PCR. C, D The proliferation of sh-SerpinB7 keratinocytes was evaluated with a CCK8 (Cell Counting Kit 8) assay and colony formation assay. E Identical fields scratch of undifferentiated sh-SerpinB7 and control NHEKs at 0 and 24 h. The dotted line represents the area of the scratch. F The mRNA level of SerpinB7 in Serpinb7^-/- and Serpinb7^+/+mice primary keratinocytes (MKs) was measured by RT-PCR. G The proliferation of SerpinB7^+/+ and Serpinb7^-/- MKs was evaluated with a CCK8 assay. H, I SerpinB7^+/+ and Serpinb7^-/- MKs homeostasis and treated for 24 h with 1.6 mM CaCl²⁺ were analyzed by RT-PCR for the expression of early (Krt1, Krt10) and late (Notch1, Loricrin, Filaggrin, Lce1a2, Lce1d, Lce1m) differentiation genes. J Morphology of SerpinB7^+/+ and Serpinb7^-/- MKs in response to Ca²⁺ induced differentiation, red arrow indicated typical undifferentiated keratinocyte state. Mean ± SD. *P < 0.05; **P < 0.01; ***P < 0.001. Two-tailed Student’s t-test (A, H, I), one-way ANOVA (B, C, F, G). All the data are representative of three independent experiments.