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Involvement of AP-1 in p38MAPK signaling pathway in osteoblast apoptosis induced by high glucose

Z P Feng1, H C Deng2, R Jiang2

  • 1Department of Endocrinology, The First Affiliated Hospital, Chongqing Medical University, Chongqing, China fengzhengping_f@yeah.net.

Genetics and Molecular Research : GMR
|May 13, 2015
PubMed

Insights

High glucose induces osteoblast apoptosis via p38MAPK/AP-1 signaling. Inhibiting this pathway with p38MAPK-shRNA reduces high glucose-induced osteoblast apoptosis, offering a potential therapeutic target.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • High glucose levels are implicated in various cellular dysfunctions.
  • Osteoblast apoptosis contributes to bone pathologies.
  • The p38 mitogen-activated protein kinase (MAPK) and activator protein-1 (AP-1) signaling pathway plays a role in cellular stress responses.

Purpose of the Study:

  • To investigate the role of the p38MAPK/AP-1 signaling pathway in high glucose-induced osteoblast apoptosis.
  • To determine if inhibiting p38MAPK can mitigate high glucose-induced osteoblast apoptosis.

Main Methods:

  • Osteoblasts (MC3T3-E1) were cultured and treated with high glucose, p38MAPK-shRNA, p38MAPK inhibitor, or control.
  • Apoptosis was assessed using TUNEL and flow cytometry.
  • Protein levels of p38MAPK and AP-1 activity were measured via Western blot and electrophoretic mobility shift assay, respectively.

Main Results:

  • High glucose significantly induced apoptosis in MC3T3-E1 osteoblasts.
  • High glucose treatment activated both p38MAPK and AP-1 signaling.
  • p38MAPK-shRNA transfection and p38MAPK inhibitor treatment effectively blocked high glucose-induced apoptosis and pathway activation.
  • Unrelated shRNA had no significant effect.

Conclusions:

  • The p38MAPK-AP-1 signaling pathway is critically involved in high glucose-induced osteoblast apoptosis.
  • Inhibition of the p38MAPK-AP-1 pathway represents a potential strategy to reduce high glucose-induced osteoblast apoptosis.

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