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Cyclic AMP, early response gene expression, and DNA synthesis in rat smooth muscle cells

A Hultgãrdh-Nilsson1, V Querol-Ferrer, B Jonzon

  • 1Department of Cell and Molecular Biology, Medical Nobel Institute, Karolinska Institutet, Stockholm, Sweden.

Experimental Cell Research
|September 1, 1994
PubMed

Insights

Neonatal and adult rat smooth muscle cells (SMC) show different growth responses to cyclic adenosine monophosphate (cAMP). cAMP inhibits adult SMC DNA synthesis but not neonatal, suggesting cAMP does not directly impact early response genes in this growth difference.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Physiology

Background:

  • Smooth muscle cells (SMC) from neonatal and adult rats exhibit distinct growth patterns.
  • Neonatal SMC growth relies on autocrine stimulation, while adult SMC require external mitogens.
  • Elevated cyclic adenosine monophosphate (cAMP) inhibits adult SMC DNA synthesis but not neonatal SMC DNA synthesis.

Purpose of the Study:

  • To investigate if differential sensitivity to cAMP in rat SMC growth is linked to early response genes.
  • To explore the impact of cAMP on gene expression in neonatal versus adult SMC.

Main Methods:

  • Isolated neonatal and adult rat SMC were treated with N-ethyl-carboxamido adenosine (NECA) to increase intracellular cAMP levels.
  • Quantitative analysis of c-jun, c-fos, c-myc, and alpha-actin mRNA expression.
  • Assessment of DNA synthesis and cell proliferation in adult SMC under NECA treatment and serum stimulation.

Main Results:

  • NECA-induced cAMP increase led to c-jun and c-fos mRNA accumulation in both neonatal and adult SMC.
  • NECA decreased c-myc mRNA in neonatal SMC but slightly increased it in adult SMC.
  • NECA did not inhibit DNA synthesis in actively proliferating adult SMC, suggesting cAMP's effect occurs in early G1 phase entry.

Conclusions:

  • The growth-inhibitory effect of NECA is unlikely to be mediated by direct actions of cAMP on early response genes.
  • While jun/fos transcription factors increase, their role in growth suppression via other genes remains a possibility.

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