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Updated: Jun 14, 2025

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
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Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

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PIN1‑silencing mitigates keratinocyte proliferation and the inflammatory response in psoriasis by activating

Shuang Xia1, Jin Li1, Hongshan Yuan1

  • 1Department of Dermatology, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu 210001, P.R. China.

Experimental and Therapeutic Medicine
|September 5, 2024
PubMed

Insights

Peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1 (PIN1) is elevated in psoriasis. Inhibiting PIN1 reduces skin cell overgrowth and inflammation by enhancing mitochondrial autophagy.

Area of Science:

  • Dermatology
  • Molecular Biology
  • Cell Biology

Background:

  • Peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1 (PIN1) is implicated in skin diseases.
  • The specific role and mechanisms of PIN1 in psoriasis pathogenesis are not well understood.

Purpose of the Study:

  • To investigate the role and molecular mechanism of PIN1 in psoriasis using an in vitro model.
  • To determine the effect of PIN1 inhibition on keratinocyte hyperproliferation, inflammation, and mitochondrial autophagy.

Main Methods:

  • HaCaT cells were stimulated with five cytokines (M5) to mimic psoriatic conditions.
  • PIN1 expression, cell proliferation, inflammatory markers, and mitochondrial autophagy were assessed using RT-qPCR, Western blotting, CCK-8 assay, EdU staining, ELISA, immunofluorescence, and JC-1 assay.
  • The effects of PIN1 silencing and a mitochondrial autophagy inhibitor (Mdivi-1) were evaluated.

Main Results:

  • PIN1 expression was significantly upregulated in M5-induced HaCaT cells.
  • PIN1 silencing suppressed M5-induced keratinocyte hyperproliferation and inflammation while promoting mitochondrial autophagy.
  • Inhibition of mitochondrial autophagy reversed the protective effects of PIN1 interference.

Conclusions:

  • PIN1 is upregulated in psoriatic inflammation-like conditions in HaCaT cells.
  • PIN1 inhibition confers protection against hyperproliferation and inflammatory injury by activating mitochondrial autophagy.
  • Targeting PIN1 may represent a therapeutic strategy for psoriasis.
Keywords:
NIMA-interacting 1inflammatory responsekeratinocytemitochondrial autophagypeptidyl-prolyl cis/trans isomeraseproliferationpsoriasis

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