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In Vivo Vascular Permeability Detection in Mouse Submandibular Gland
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Increased microvascular permeability in mice lacking Epac1 (Rapgef3).

R K Kopperud1,2, C Brekke Rygh1, T V Karlsen1

  • 1Department of Biomedicine, University of Bergen, Bergen, Norway.

Acta Physiologica (Oxford, England)
|April 21, 2016
PubMed
Summary

The study found that Epac1 (Exchange protein directly activated by cAMP 1) normally restricts blood vessel permeability. Mice lacking Epac1 showed increased leakage, suggesting Epac1 maintains vascular integrity.

Keywords:
Epac deletion (mouse)Rapgefatrial natriuretic peptidecAMPendothelial junctionmicrovascular permeability (in vivo)

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Area of Science:

  • Physiology
  • Molecular Biology
  • Vascular Biology

Background:

  • Endothelial macromolecule permeability is critical for maintaining blood and extracellular volume.
  • Cyclic adenosine monophosphate (cAMP) signaling pathways regulate vascular permeability.
  • Rap guanine nucleotide exchange factors, Epac1 and Epac2, are key mediators of cAMP signaling.

Purpose of the Study:

  • To investigate the in vivo role of Epac1 and Epac2 in controlling basal microvascular macromolecule permeability.
  • To determine if Epac1 or Epac2 influence transvascular flux under normal physiological conditions.

Main Methods:

  • Generation and comparison of Epac1 knockout (Epac1-/-) and Epac2 knockout (Epac2-/-) mice with wild-type littermates.
  • Quantification of transvascular albumin flux in various tissues using radiolabeled albumin.
  • Assessment of vascular leakage using dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) with Gadomer-17.

Main Results:

  • Epac1-/- mice exhibited significantly increased basal transvascular macromolecule transport compared to wild-type mice.
  • The absence of Epac1 led to reduced vascular permeability responses to atrial natriuretic peptide (ANP).
  • Ultrastructural analysis of Epac1-/- microvessels revealed less organized interendothelial junctions.

Conclusions:

  • Epac1 plays a tonic inhibitory role in regulating basal microvascular permeability in vivo.
  • Loss of Epac1 function increases baseline vascular permeability by affecting interendothelial junctions.
  • Epac1 activity may be involved in the mechanism by which ANP increases vascular permeability.