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JNK/ATF2 pathway is involved in iodinated contrast media-induced apoptosis

Hsiang-Chun Lee1, Sheng-Hsiung Sheu, Hsueh-Wei Yen

  • 1Division of Cardiology, Department of Internal Medicine, Kaohsiung Medical University Hospital, No. 100 Tz-You 1st Road, Kaohsiung, Taiwan, ROC.

American Journal of Nephrology
|November 20, 2009
PubMed
Abstract

Insights

Activating transcriptional factor 2 (ATF2) plays a protective role in contrast media-induced nephropathy. Lowering ATF2 levels exacerbates kidney cell death, suggesting ATF2 is a key factor in preventing kidney damage from contrast agents.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Cellular Biology

Background:

  • Activating transcriptional factor 2 (ATF2), a gene involved in histone modification, is implicated in oxidative stress-induced apoptosis.
  • Contrast media-induced nephropathy (CMN) is a significant clinical concern.
  • The precise role of ATF2 in CMN remains unclear.

Purpose of the Study:

  • To investigate the role of ATF2 in the development of contrast media-induced nephropathy.
  • To determine how different types of contrast media affect ATF2 expression and activity.

Main Methods:

  • Human embryonic kidney 293T cells were exposed to various contrast media (diatrizoate, iothalamate, iohexol, iodixanol).
  • ATF2 mRNA expression and phosphorylation were analyzed using real-time PCR and Western blotting.
  • ATF2 was knocked down using short interfering RNA.
  • Wistar rats received diatrizoate or saline, and kidney tubular cell apoptosis was assessed via TUNEL staining.

Main Results:

  • Diatrizoate, iodixanol, and iothalamate induced ATF2 mRNA expression and phosphorylation in kidney cells in a time-dependent manner.
  • Diatrizoate administration led to significantly more apoptotic kidney cells compared to saline.
  • Knockdown of ATF2 exacerbated cell death in the presence of diatrizoate, indicating a protective function of ATF2.

Conclusions:

  • The differential activation of ATF2 by various contrast media offers new insights into CMN mechanisms.
  • ATF2 appears to have a protective role against contrast media-induced kidney injury.
  • Targeting ATF2 may represent a novel strategy for preventing CMN.

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