Related Experiment Video

Updated: May 5, 2026

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice
07:21

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

Published on: September 28, 2015

39.9K

TGF-beta activity protects against inflammatory aortic aneurysm progression and complications in angiotensin

Yu Wang1, Hafid Ait-Oufella, Olivier Herbin

  • 1INSERM U970, Paris Cardiovascular Research Center, Université Paris-Descartes and Assistance Publique-Hôpitaux de Paris, Paris, France.

The Journal of Clinical Investigation
|January 27, 2010
PubMed

Insights

Transforming growth factor-beta (TGF-β) neutralization increases susceptibility to abdominal aortic aneurysm (AAA) in mice. This study reveals TGF-β’s protective role in innate immunity and vessel integrity, contrasting its role in Marfan syndrome.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Vascular Biology

Background:

  • Abdominal aortic aneurysm (AAA) poses a significant mortality risk, particularly in elderly men.
  • Angiotensin II (Ang II)-dependent TGF-β activity is implicated in aortic aneurysm progression in Marfan syndrome.
  • The specific role of TGF-β in experimental AAA models remains incompletely understood.

Purpose of the Study:

  • To comprehensively assess the role of TGF-β in experimental models of Ang II-induced AAA.
  • To investigate the impact of TGF-β neutralization on AAA formation and complications in normocholesterolemic mice.

Main Methods:

  • Systemic neutralization of TGF-β activity in normocholesterolemic C57BL/6 mice subjected to Ang II infusion.
  • Echographic assessment of aneurysm complications (fissuration, double channel formation, rupture).
  • Evaluation of immune cell involvement (T cells, B cells, monocytes) and specific molecular pathways (IFN-γ, IL-4, IL-6, TNF-α, CX3CR1, MMP-12).

Main Results:

  • TGF-β neutralization significantly increased susceptibility to Ang II-induced AAA formation and complications, including rupture and death.
  • Aneurysm development was refractory to inhibition of IFN-γ, IL-4, IL-6, or TNF-α signaling.
  • Monocyte depletion and MMP-12 deficiency markedly inhibited AAA progression and rupture, respectively, while TGF-β neutralization enhanced monocyte invasiveness and MMP-12 activity.

Conclusions:

  • TGF-β plays a critical role in modulating the innate immune response and maintaining vascular integrity in C57BL/6 mice, protecting against AAA.
  • This protective role contrasts with the previously reported pathogenic role of TGF-β in Marfan syndrome-associated AAA.
  • Targeting TGF-β may exacerbate AAA, highlighting its complex involvement in vascular disease pathogenesis.

More Related Videos

Ultrasound Imaging of the Thoracic and Abdominal Aorta in Mice to Determine Aneurysm Dimensions06:08

Ultrasound Imaging of the Thoracic and Abdominal Aorta in Mice to Determine Aneurysm Dimensions

Published on: March 8, 2019

20.4K
Drug Treatment by Central Venous Catheter in a Mouse Model of Angiotensin II Induced Abdominal Aortic Aneurysm and Monitoring by 3D Ultrasound10:09

Drug Treatment by Central Venous Catheter in a Mouse Model of Angiotensin II Induced Abdominal Aortic Aneurysm and Monitoring by 3D Ultrasound

Published on: August 4, 2022

4.6K

Related Concept Videos

TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
7.2K