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Protein kinase C inhibitors decrease endothelin ET(B) receptor mRNA expression and contraction during organ culture

Erik Uddman1, Mikael Adner, Lars Edvinsson

  • 1Department of Internal Medicine, Lund University Hospital, Lund, Sweden. Erik.Uddman@med.lu.se

Insights

Protein kinase C (PKC) inhibitors reduce endothelin ET(B) receptor upregulation in rat arteries cultured ex vivo. This suggests PKC plays a role in increasing these receptors during organ culture.

Area of Science:

  • Vascular Biology
  • Pharmacology
  • Molecular Biology

Background:

  • Endothelin ET(B) receptors mediate vasoconstriction.
  • Organ culture can alter receptor expression in arterial segments.
  • Protein kinase C (PKC) is a key signaling pathway in cells.

Purpose of the Study:

  • To investigate the role of PKC in endothelin ET(B) receptor upregulation during organ culture of rat mesenteric arteries.
  • To determine the effect of specific PKC inhibitors on receptor-mediated contraction and mRNA expression.

Main Methods:

  • Isolated rat mesenteric artery segments were maintained in organ culture for 24 hours.
  • Contractile responses to endothelin ET(B) receptor agonist sarafotoxin 6c (S6c) were measured.
  • PKC inhibitors (staurosporine, K252a, Ro31-7549) were applied during preincubation or 24-hour treatment.
  • Endothelin ET(B) receptor mRNA expression was analyzed using real-time PCR.

Main Results:

  • Organ culture significantly increased S6c-induced contraction, indicating ET(B) receptor upregulation.
  • PKC inhibitors staurosporine and K252a reduced this enhanced contraction.
  • The PKC inhibitor Ro31-7549 abolished the upregulation after 24-hour treatment.
  • PKC inhibition also abolished the increased mRNA expression of endothelin ET(B) receptors.

Conclusions:

  • PKC signaling is involved in the upregulation of endothelin ET(B) receptors in rat mesenteric arteries during organ culture.
  • PKC inhibitors can prevent the increase in receptor expression and function under these conditions.

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