Peptidyl‑prolyl cis/trans isomerase, NIMA-interacting 1 (PIN1) has been suggested to be a critical regulator in skin‑related diseases. However, the role and molecular mechanism of PIN1 in psoriasis remain unclear. HaCaT cells were stimulated with five cytokines (M5) to induce psoriatic inflammation‑like conditions. Reverse transcription‑quantitative PCR and western blotting were performed to examine PIN1 expression in M5‑induced HaCaT cells. A Cell Counting Kit‑8 assay and 5‑ethynyl‑2'‑deoxyuridine staining were employed to examine cell proliferation. Inflammatory factors were evaluated using ELISA kits and western blot analysis. Mitochondrial autophagy was examined by immunofluorescence staining, western blotting and a JC‑1 assay. Western blot analysis was adopted to assess the levels of psoriasis marker proteins. PIN1 expression was markedly elevated in M5‑induced HaCaT cells. Silencing of PIN1 inhibited M5‑induced hyperproliferation and the inflammatory response, while it promoted mitochondrial autophagy in HaCaT cells. The addition of the mitochondrial autophagy inhibitor mitochondrial division inhibitor‑1 reversed the effects of PIN1 interference on proliferation, the inflammatory response and mitochondrial autophagy in M5‑induced HaCaT cells. The present study revealed that PIN1 inhibition protected HaCaT cells against M5‑induced hyperproliferation and inflammatory injury through the activation of mitochondrial autophagy.

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