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PIN1 Suppresses the Hepatic Differentiation of Pulp Stem Cells via Wnt3a

H J Kim1, Y A Cho2, Y M Lee2

  • 11 Department of Oral Physiology, BK21 PLUS Project, and Institute of Translational Dental Sciences, School of Dentistry, Pusan National University, Yangsan, Republic of Korea.

Journal of Dental Research
|July 22, 2016
PubMed

Insights

PIN1 inhibition promotes liver stem cell differentiation via the Wnt/β-catenin pathway. Combining this inhibition with stem cell therapy effectively treats liver fibrosis in mice.

Area of Science:

  • Stem cell biology
  • Hepatology
  • Molecular biology

Background:

  • Liver fibrosis is a significant health concern.
  • Human dental pulp stem cells (hDPSCs) show potential for regenerative medicine.
  • The role of Peptidylprolyl cis-trans isomerase NIMA-interacting 1 (PIN1) in hepatic differentiation is not well understood.

Purpose of the Study:

  • To investigate PIN1's role in hDPSC hepatic differentiation.
  • To explore the therapeutic potential of hDPSC transplantation combined with PIN1 inhibition for liver fibrosis.

Main Methods:

  • In vitro studies using adenovirus-mediated PIN1 overexpression and PIN1 inhibitor juglone.
  • In vivo studies involving carbon tetrachloride (CCl4)-induced liver fibrosis in mice.
  • Assessment of hepatic differentiation markers and liver function tests.

Main Results:

  • PIN1 overexpression suppressed hDPSC hepatic differentiation, while juglone promoted it by downregulating Wnt3a and β-catenin.
  • Combined hDPSC transplantation and juglone treatment significantly reduced liver fibrosis in mice.
  • This combination therapy restored serum levels of alanine transaminase, aspartate transaminase, and ammonia.

Conclusions:

  • PIN1 inhibition promotes hDPSC hepatic differentiation through the Wnt/β-catenin pathway.
  • Combined hDPSC transplantation and PIN1 inhibition demonstrate a novel therapeutic strategy for liver fibrosis.
  • This approach offers a potential new treatment for liver injury.
Keywords:
NIMA-interacting peptidylprolyl isomeraseWnt3adental pulpdifferentiationhepatocytesliver fibrosis

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