Synapse
⌘+K
Synapse
PulseExploreClubsResearchersJournals
Instagram
HomeClubsExplore
June 9, 2009Journal of Clinical InvestigationOpen Access

The natriuretic peptide/guanylyl cyclase–A system functions as a stress-responsive regulator of angiogenesis in mice

View Full Paper
Ask AI
Bookmark
Share

Key result

Global and endothelial deletion of the guanylyl cyclase-A receptor severely impaired blood flow recovery and angiogenesis after hind limb ischemia in mice.

Why the study?

Does the natriuretic peptide/GC-A system regulate angiogenesis in response to ischemia or pressure overload in mice?

Population

Mice with global, endothelial cell-restricted, or smooth muscle cell-restricted deletion of the GC-A gene…

Comparison

Hind limb ischemia or transverse aortic… vs Wild-type/control mice undergoing the same…

Design

Preclinical

Follow-up

up to 35 days

Authors

MKMichaela KühnHeart Failure & TransplantKVKatharina VölkerUniversity of WürzburgKSKristine SchwarzUniversity of Würzburg

Discussion

Loading...

Member takes

Implication

No immediate clinical implications; hypothesis-generating for endothelial GC-A in ischemic angiogenesis.

Structured PICO

Does the natriuretic peptide/GC-A system regulate angiogenesis in response to ischemia or pressure overload in mice?

P
Population
Mice with global, endothelial, or smooth muscle-restricted deletion of guanylyl cyclase-A subjected to hind limb ischemia or transverse aortic constriction.
E
Exposure
Hind limb ischemia (femoral artery excision) or transverse aortic constriction (TAC); in vitro treatment with B-type natriuretic peptide (BNP) or atrial natriuretic peptide (ANP).
C
Comparator
Wild-type/control mice undergoing the same procedures; untreated cells or cells treated with inhibitors (e.g., PKG I inhibitor).
O
Outcome
Vascular regeneration (blood flow recovery by laser Doppler perfusion imaging, collateral vessel formation by magnetic resonance angiography, and capillary density) and cardiac angiogenesis/hypertrophy.surrogate

Main Result

Absolute Event Rate: 0.51% vs 0.85%

p-value: p=0.0001

BNP acts as a paracrine regulator of vascular regeneration and angiogenesis via the endothelial GC-A receptor in response to ischemia and mechanical stress.

Limitations

  • Animal model findings may not directly translate to human cardiovascular diseases
  • Laser Doppler measurements were restricted to superficial skin blood flow

Cite This Study

Kühn et al. (2009) studied Hind limb ischemia and cardiac hypertrophy. Guanylyl cyclase-A (GC-A) deletion vs. Wild-type/control littermates was evaluated on Ratio of perfusion in ischemic relative to nonischemic hind limb at day 35 (p=0.0001). Global and endothelial deletion of the guanylyl cyclase-A receptor severely impaired blood flow recovery and angiogenesis after hind limb ischemia in mice.

synapsesocial.com/papers/6a7c5a6a0449e558d7c2ea0ahttps://doi.org/10.1172/jci37430
View Full Paper
Ask AI
Bookmark
Share

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Natriuretic Peptide Family as a Novel Antimigration Factor of Vascular Smooth Muscle Cells1997 · 48 citations
  2. 2Natriuretic Peptides Inhibit DNA Synthesis in Cardiac Fibroblasts1995 · 273 citations
  3. 3Angiotensin II Type 2 Receptor Inhibits Vascular Endothelial Growth Factor–Induced Migration and In Vitro Tube Formation of Human Endothelial Cells2003 · 123 citations
  4. 4Vascular endothelium is critically involved in the hypotensive and hypovolemic actions of atrial natriuretic peptide2005 · 171 citations
  5. 5Smooth muscle-selective deletion of guanylyl cyclase-A prevents the acute but not chronic effects of ANP on blood pressure2002 · 342 citations