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Transient co-localization of c-Jun N-terminal kinase and c-Jun with heat shock protein 70 in pulp cells during

C Kitamura1, Y Ogawa, T Nishihara

  • 1Department of Operative Dentistry and Endodontics, Kyushu Dental College, 2-6-1 Manazuru, Kokurakita, Kitakyushu 803-8580, Japan. chi-aki-k@kyu-dent.ac.jp

Journal of Dental Research
|February 4, 2003
PubMed

Insights

The c-Jun N-terminal kinase (JNK) pathway and heat-shock proteins (HSPs) influence pulp cell apoptosis during wound healing. HSP70 may inhibit JNK-induced apoptosis, aiding pulp repair.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Immunology

Background:

  • The c-Jun N-terminal kinase (JNK) pathway and heat-shock proteins (HSPs) are implicated in stress-induced apoptosis.
  • Pulp apoptosis is a critical factor in dental wound healing.

Purpose of the Study:

  • To investigate the roles of JNK, c-Jun, and anti-apoptotic HSPs in pulp apoptosis during wound healing.
  • To elucidate the interaction between JNK signaling and HSP70 in regulating pulp cell fate.

Main Methods:

  • Immunohistochemistry to detect active JNK, c-Jun, and HSP70 expression in pulp tissue.
  • Analysis of protein localization and co-localization within pulp cells post-injury.
  • Assessment of cellular apoptosis in relation to protein expression patterns.

Main Results:

  • JNK and c-Jun activation correlated with pulp cell apoptosis one day after injury.
  • HSP70 was initially found in non-apoptotic cells and translocated to nuclei, co-localizing with JNK and c-Jun.
  • HSP70 relocated to the cytoplasm as JNK and c-Jun expression diminished, suggesting a protective role.

Conclusions:

  • The JNK pathway is a key mediator of apoptosis in pulp cells during wound healing.
  • HSP70 exhibits an inhibitory effect on JNK-induced pulp cell apoptosis, potentially promoting tissue repair.

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