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Updated: Jun 3, 2026

Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes
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Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes

Published on: January 7, 2013

Involvement of PI3K/Akt/CREB and redox changes in mitochondrial defect of osteoblastic MC3T3-E1 cells

Eun Mi Choi1, Young Soon Lee

  • 1Department of Food and Nutrition, Kyung Hee University, 1, Hoegi-Dong, Dongdaemun-gu, Seoul 130-701, Republic of Korea. cheunmi@hanmail.net

Toxicology in Vitro : an International Journal Published in Association with BIBRA
|April 7, 2011
PubMed

Insights

Antimycin A damages osteoblasts by inhibiting mitochondrial electron transport. This leads to reduced pyridine nucleotides (NAD+ and NADPH) and impaired PI3K/Akt/CREB signaling, impacting osteoblast function.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Mitochondrial Biology

Background:

  • Antimycin A (AMA) inhibits mitochondrial electron transport at complex III.
  • Understanding AMA's cellular damage mechanisms is crucial for osteoblast health.

Purpose of the Study:

  • To investigate the mechanisms underlying Antimycin A-induced cell damage in osteoblasts.
  • To explore the role of pyridine nucleotides and the PI3K/Akt/CREB pathway in AMA's effects.

Main Methods:

  • Treatment of MC3T3-E1 osteoblastic cells with Antimycin A.
  • Measurement of cellular levels of adenosine 3',5'-cyclic monophosphate (cAMP), NAD+, NADH, NADP+, and NADPH.
  • Assay of phosphoinositide 3-kinase (PI3K), Akt, phosphorylated CREB, aconitase, and thioredoxin reductase activities.

Main Results:

  • AMA treatment decreased cAMP levels, PI3K, Akt, and phosphorylated CREB.
  • AMA significantly reduced NAD+ and NADPH levels in osteoblasts.
  • Activities of aconitase and thioredoxin reductase were diminished by AMA.

Conclusions:

  • The PI3K/Akt/CREB pathway is implicated in Antimycin A-induced osteoblast damage.
  • Pyridine nucleotides (NAD+ and NADPH) are involved in the mitochondrial dysfunction caused by AMA.
  • AMA affects osteoblast mitochondrial function through these pathways.

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