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All-trans retinoic acid regulates c-jun expression via ERK5 in cardiac myoblasts

Xia Ren1, Xi Ma, Yong Li

  • 1Laboratory of Development Molecular Biology, Department of Nutrition and Food Hygiene, School of Public Health, Peking University Health Science Center, Beijing 100083, PR China.

The Journal of Nutritional Biochemistry
|May 19, 2007
PubMed

Insights

Retinoic acid (RA) promotes H9c2 cell proliferation by increasing c-jun expression. The ERK5 pathway, not ERK1, mediates this effect, suggesting its role in heart development.

Area of Science:

  • Cardiovascular Biology
  • Cellular Signaling
  • Developmental Biology

Background:

  • Retinoic acid (RA), a vitamin A metabolite, is crucial for cell proliferation.
  • Mitogen-activated protein kinases (MAPKs) are key regulators of cardiac cellular processes.

Purpose of the Study:

  • To investigate if all-trans retinoic acid (atRA) influences H9c2 rat ventricular cell proliferation.
  • To determine the involvement of the ERK (extracellular signal-regulated kinase) family in atRA-mediated proliferation.

Main Methods:

  • H9c2 cells were cultured and assessed for proliferation using MTT and (3)H-thymidine incorporation assays.
  • Luciferase reporter gene and Western blot assays were employed to measure c-jun transcription and protein levels.
  • ERK5 and ERK1 activity and subcellular localization were analyzed via Western blot and confocal microscopy.

Main Results:

  • atRA (0.05 microM) enhanced H9c2 cell proliferation and increased c-jun transcription and protein expression.
  • Inhibition of ERK5 significantly reduced atRA-induced pJluc expression (P<.01).
  • atRA induced ERK5 activity and promoted its nuclear translocation, while ERK1 activity and translocation remained unaffected.

Conclusions:

  • The ERK5 signaling pathway appears to mediate the proliferative effects of atRA in H9c2 myocardial cells.
  • These findings suggest a role for the ERK5 pathway in retinoic acid-regulated heart development.

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