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Updated: Jul 13, 2026

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice

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Published on: September 28, 2015

Antiangiogenic effect of angiotensin II type 2 receptor in ischemia-induced angiogenesis in mice hindlimb.

Jean-Sébastien Silvestre¹, Radia Tamarat, Takaaki Senbonmatsu

¹INSERM U541, Hôpital Lariboisière, IFR Circulation-Lariboisière, Université Paris 7-Denis Diderot, Paris, France.

Circulation Research

|June 1, 2002

Summary

The angiotensin II type 2 (AT(2)) receptor negatively impacts blood vessel growth after hindlimb ischemia. Blocking this receptor enhances angiogenesis and reduces cell death, suggesting a therapeutic target for ischemic diseases.

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Published on: September 28, 2015

Assessing Therapeutic Angiogenesis in a Murine Model of Hindlimb Ischemia

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Published on: June 8, 2019

A Modified Surgical Model of Hind Limb Ischemia in ApoE-/- Mice using a Miniature Incision

A Modified Surgical Model of Hind Limb Ischemia in ApoE^-/- Mice using a Miniature Incision

Published on: May 13, 2021

Area of Science:

Cardiovascular Research
Molecular Biology
Regenerative Medicine

Background:

Angiotensin II signaling pathways are crucial in cardiovascular regulation.
The role of the angiotensin type 2 (AT(2)) receptor in angiogenesis remains incompletely understood.
Hindlimb ischemia is a condition characterized by impaired blood flow, leading to tissue damage.

Purpose of the Study:

To investigate the specific role of the AT(2) receptor in ischemia-induced angiogenesis.
To determine the impact of AT(2) receptor deletion on revascularization following surgical hindlimb ischemia.
To elucidate the molecular mechanisms underlying AT(2) receptor modulation of angiogenesis and cell survival.

Main Methods:

Surgically induced hindlimb ischemia model in wild-type and AT(2) gene-deleted (Agtr2(-)/Y) mice.
Quantification of angiogenesis using microangiography, capillary density, and laser Doppler perfusion imaging.
Western blot analysis for vascular endothelial growth factor (VEGF), eNOS, Bax, and Bcl-2; RT-PCR for AT(2) mRNA; TUNEL assay for cell death.

Main Results:

AT(2) receptor deletion significantly improved angiogenesis and blood perfusion in ischemic hindlimbs compared to controls.
Revascularization in AT(2)-deficient mice was associated with increased Bcl-2 (anti-apoptotic) and decreased cell death.
Angiotensin II treatment enhanced angiogenesis in wild-type mice but did not affect the robust response in AT(2)-deficient mice.

Conclusions:

The AT(2) receptor subtype negatively modulates ischemia-induced angiogenesis.
This negative regulation appears to occur through the activation of apoptotic processes.
Targeting the AT(2) receptor may represent a novel therapeutic strategy to promote revascularization in ischemic conditions.