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Auto/Paracrine C-Type Natriuretic Peptide/Cyclic GMP Signaling Prevents Endothelial Dysfunction.

Franziska Werner1, Takashi Naruke1, Lydia Sülzenbrück1

  • 1Institute of Physiology, University Würzburg, 97070 Würzburg, Germany.

International Journal of Molecular Sciences
|July 27, 2024
PubMed
Summary
This summary is machine-generated.

Endothelial C-type natriuretic peptide (CNP) signaling protects female mice from cardiovascular disease. Deleting its receptor (GC-B) in endothelial cells worsened arterial stiffness, hypertension, and atherosclerosis.

Keywords:
C-type natriuretic peptideangiogenesisarterial stiffeningatherosclerosiscyclic GMPendothelial dysfunctionsystolic hypertension

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Area of Science:

  • Cardiovascular Biology
  • Endothelial Function
  • Molecular Signaling

Background:

  • Endothelial dysfunction is central to cardiovascular diseases.
  • C-type natriuretic peptide (CNP) is an endothelial hormone regulating vascular tone and barrier function.
  • The guanylyl cyclase-B (GC-B) receptor mediates CNP's effects and is expressed in endothelial cells.

Purpose of the Study:

  • To investigate the role of endothelial CNP/cGMP signaling in cardiovascular health and disease.
  • To characterize the impact of endothelial-selective GC-B deletion on vascular function and disease progression.
  • To explore potential sex-specific differences in CNP/GC-B signaling pathways.

Main Methods:

  • Generated mice with endothelial-selective deletion of the GC-B receptor (EC GC-B KO).
  • Assessed vascular structure, function, and inflammatory markers in EC GC-B KO mice.
  • Evaluated atherosclerosis development in EC GC-B KO and control mice on an Ldlr-deficient background.
  • Studied vascular regeneration capacity following hind-limb ischemia.

Main Results:

  • EC GC-B KO mice exhibited thicker, stiffer aortae and isolated systolic hypertension.
  • Increased expression of proinflammatory markers (E-selectin, VCAM-1) and impaired nitric oxide bioavailability were observed.
  • Enhanced atherosclerosis, characterized by larger plaque areas, increased macrophage infiltration, and necrotic cores, was found in double KO mice.
  • Diminished vascular regeneration was noted in EC GC-B KO mice.
  • All observed changes were specific to female mice, with no significant effects in males.

Conclusions:

  • Endothelial CNP/GC-B/cGMP signaling is crucial for protecting against arterial stiffness, systolic hypertension, and atherosclerosis.
  • This signaling pathway also plays a vital role in promoting reparative angiogenesis.
  • A significant sex disparity exists, with diminished CNP/GC-B activity predominantly impacting endothelial dysfunction in female mice.