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PKC-zeta expression is lower in osteoblasts from arthritic patients: IL1-beta and TNF-alpha induce a similar decrease

Nicoletta Zini1, Alberto Bavelloni, Gina Lisignoli

  • 1IGM-CNR, Sezione di Bologna c/o IOR, via di Barbiano 1/10, 40136 Bologna, Italy.

Journal of Cellular Biochemistry
|June 2, 2007
PubMed

Insights

Osteoarthritis and rheumatoid arthritis patients show altered Protein Kinase C (PKC) isoform expression in osteoblasts. Proinflammatory cytokines like IL-1beta and TNF-alpha decrease PKC-zeta, mimicking changes seen in arthritis.

Area of Science:

  • Biochemistry and Molecular Biology
  • Cell Biology
  • Immunology

Background:

  • Protein Kinase C (PKC) is a crucial enzyme family regulating diverse cellular functions.
  • PKC isoforms play significant roles in cell proliferation, differentiation, and signal transduction.
  • Dysregulation of PKC signaling is implicated in various pathological conditions, including inflammatory diseases.

Purpose of the Study:

  • To investigate the expression patterns of 11 Protein Kinase C (PKC) isoforms in osteoblasts from patients with osteoarthritis (OA) and rheumatoid arthritis (RA).
  • To compare PKC isoform expression in arthritic osteoblasts with those from post-traumatic (PT) patients.
  • To determine the effect of proinflammatory cytokines on PKC isoform expression in osteoblasts.

Main Methods:

  • Western blotting was employed to analyze the expression of nine PKC isoforms in osteoblasts.
  • Immuno-electron microscopy was used to confirm subcellular distribution and quantitative differences.
  • Osteoblasts were treated with interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) to assess cytokine effects.

Main Results:

  • Nine PKC isoforms were detected in osteoblasts: -alpha, -beta(I), -beta(II), -delta, -theta, -epsilon, -zeta, -iota/lambda, and -micro.
  • Osteoarthritis and rheumatoid arthritis patients exhibited increased expression of PKC-theta and -micro, alongside decreased expression of PKC-epsilon and -zeta compared to normal cells.
  • Treatment with IL-1β and TNF-α significantly reduced PKC-zeta expression in post-traumatic osteoblasts, mirroring findings in arthritic patients.

Conclusions:

  • Specific PKC isoforms show altered expression in osteoblasts from patients with osteoarthritis and rheumatoid arthritis.
  • Proinflammatory cytokines, such as IL-1β and TNF-α, can modulate PKC-zeta expression in osteoblasts.
  • These findings suggest a potential role for PKC signaling dysregulation in the pathogenesis of arthritis.

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