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Related Concept Videos

Aneurysm I: Introduction01:30

Aneurysm I: Introduction

An aortic aneurysm is a localized outpouching or dilation at a weak point in the artery wall. It may involve different parts of the aorta, such as the abdominal aorta, aortic arch, or thoracic aorta.Etiological factorsSeveral disorders are associated with aortic aneurysms.Congenital causes, such as primary connective tissue disorders like Marfan syndrome, impact the integrity and strength of connective tissues, notably affecting the aorta. Marfan syndrome is a genetic disorder that specifically...
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Updated: Jun 15, 2026

Murine Surgical Model of Topical Elastase Induced Descending Thoracic Aortic Aneurysm
08:33

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Cellular phenotype transformation occurs during thoracic aortic aneurysm development.

Jeffrey A Jones1, Juozas A Zavadzkas, Eileen I Chang

  • 1Division of Cardiothoracic Surgery, Department of Surgery, Medical University of South Carolina, and Ralph H. Johnson Veterans Affairs Medical Center, Charleston, SC 29425, USA. jonesja@musc.edu

The Journal of Thoracic and Cardiovascular Surgery
|March 12, 2010
PubMed
Summary
This summary is machine-generated.

Thoracic aortic aneurysm fibroblasts exhibit a stable, unique gene expression profile. This altered phenotype in aortic fibroblasts drives extracellular matrix breakdown, contributing to aneurysm progression.

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Published on: September 12, 2017

Area of Science:

  • Cardiovascular Biology
  • Vascular Remodeling
  • Extracellular Matrix Dynamics

Background:

  • Thoracic aortic aneurysms (TAAs) involve complex vascular extracellular matrix remodeling.
  • Altered resident cellular function, particularly aortic fibroblasts, is implicated in TAA pathogenesis.
  • The potential for stable phenotypic changes in aortic fibroblasts during TAA formation requires investigation.

Purpose of the Study:

  • To test the hypothesis that aortic fibroblasts undergo a stable phenotypic change during TAA development.
  • To characterize the gene expression profile of aortic fibroblasts isolated from TAA models.
  • To assess the functional response of these fibroblasts to biological stimuli.

Main Methods:

  • Primary murine aortic fibroblasts were isolated from normal and TAA-induced aortas.
  • Focused polymerase chain reaction arrays analyzed the expression of 38 fibroblast-specific genes.
  • Gene expression was assessed in the absence and presence of biological stimuli (endothelin-1, phorbol-12-myristate-13-acetate, angiotensin-II).

Main Results:

  • TAA fibroblasts showed elevated expression of matrix metalloproteinases (Mmp2, Mmp11, Mmp14) and collagen/elastin genes.
  • Decreased expression of Mmp3, Timp3, and Ltbp1 was observed in TAA fibroblasts.
  • TAA fibroblast gene expression profiles differed from normal fibroblasts, even after stimulation.

Conclusions:

  • Primary aortic fibroblasts from TAA-induced mice possess a unique and stable gene expression profile.
  • These fibroblasts exhibit distinct transcriptional responses to biological stimuli compared to normal fibroblasts.
  • These findings suggest a stable phenotypic shift in aortic fibroblasts drives extracellular matrix proteolysis in TAA progression.