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Angiotensin II induces mitochondrial dysfunction and promotes apoptosis via JNK signalling pathway in primary mouse

Guangyue Li1, Min Wang1, Liang Hao1

  • 1State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, P. R. China.

Archives of Oral Biology
|March 18, 2014
PubMed
Abstract

Insights

Angiotensin II (Ang II) induces osteoblast apoptosis by impairing mitochondrial function and ATP production. This pathway involves the c-jun N-terminal kinases (JNK) signaling cascade, offering insights into bone resorption models.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Physiology

Background:

  • Osteoblasts are crucial for bone formation and maintenance.
  • Mitochondrial dysfunction is implicated in various cellular pathologies.
  • The role of Angiotensin II in osteoblast apoptosis requires further elucidation.

Purpose of the Study:

  • To investigate the impact of Angiotensin II (Ang II) on mouse calvaria osteoblast mitochondrial function, reactive oxygen species (ROS) generation, and apoptosis.
  • To explore the involvement of the c-jun N-terminal kinases (JNK) signaling pathway in Ang II-induced osteoblast apoptosis.

Main Methods:

  • Osteoblasts were isolated and treated with Ang II.
  • Mitochondrial ROS, superoxide production, and ATP levels were measured.
  • Cell proliferation, apoptosis markers (Bax, Bcl-2), and JNK pathway activation were assessed using ELISA and Western blotting.

Main Results:

  • Ang II significantly increased superoxide production and ROS generation in osteoblasts.
  • Ang II treatment led to mitochondrial membrane potential dissipation, reduced ATP levels, and induced apoptosis.
  • JNK pathway activation was identified as a key mediator in Ang II-induced, mitochondria-dependent apoptosis.

Conclusions:

  • Ang II promotes osteoblast apoptosis by suppressing mitochondrial respiration and ATP production.
  • The JNK signaling pathway plays a critical role in mediating Ang II-induced osteoblast apoptosis.
  • These findings suggest potential applications of Ang II-stimulated osteoblasts in modeling bone resorption.
Keywords:
Angiotensin II (Ang II)ApoptosisJNKMitochondriaReactive oxygen species (ROS)

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