Related Experiment Video
Updated: Jun 18, 2026
08:28
Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro
Published on: February 15, 2022
Smooth muscle phenotypic modulation is an early event in aortic aneurysms
Gorav Ailawadi1, Christopher W Moehle, Hong Pei
1Department of Surgery, University of Virginia, Charlottesville, VA 22908, USA. gorav@virginia.edu
The Journal of Thoracic and Cardiovascular Surgery
|November 26, 2009
Summary
Vascular smooth muscle cells change phenotype before aortic aneurysm formation, with reduced markers and increased matrix metalloproteinases. This suggests targeting smooth muscle cells could treat aortic aneurysms.
Area of Science:
- Vascular Biology
- Atherosclerosis Research
- Cellular Phenotypic Modulation
Background:
- Vascular smooth muscle cells (VSMCs) alter phenotype in response to injury, involving gene repression and matrix metalloproteinase (MMP) production.
- The specific role of VSMCs in aortic aneurysm development remains largely unknown.
- This study investigates VSMC phenotypic modulation during early aortic aneurysm development.
Purpose of the Study:
- To test the hypothesis that VSMCs undergo phenotypic modulation early in aortic aneurysm development.
- To characterize changes in VSMC marker gene expression and MMP production in experimental and human aortic aneurysms.
Main Methods:
- Abdominal aortas from C57B6 mice were perfused with elastase or saline and analyzed at various time points (1, 3, 7, 14 days).
- Quantitative polymerase chain reaction and immunohistochemistry were used to assess expression of VSMC markers (SM22α, smooth muscle α-actin) and MMPs (MMP-2, MMP-9).
- Human aortic aneurysms and control aortas were analyzed similarly.
Main Results:
- Elastase perfusion led to increased aortic diameter by 14 days.
- Significant reduction in SM22α and smooth muscle α-actin expression was observed by 7 days, preceding aneurysm formation.
- Increased MMP-2 and MMP-9 expression occurred at 7 and 14 days in experimental and human aneurysms compared to controls.
Conclusions:
- Aortic aneurysms are characterized by VSMC phenotypic modulation, including decreased VSMC markers and increased MMPs.
- These phenotypic changes precede aneurysm formation in experimental models.
- Modulating VSMCs towards a reparative phenotype may offer a novel therapeutic strategy for aortic aneurysms.
More Related Videos
Related Concept Videos
01:30Atherosclerosis I: Introduction
Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
01:30Aneurysm 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...
01:15Aortic Regurgitation I: Introduction
IntroductionAortic regurgitation is characterized by the backward flow of blood from the aorta into the left ventricle during diastole and arises from the improper closure of the aortic valve. This condition results in left ventricular volume overload and can stem from both acute and chronic etiologies, each contributing uniquely to the disease's progression and symptomatology.Acute and Chronic CausesAcute aortic regurgitation often results from events that suddenly impair the integrity of the...
01:25Smooth Muscle Contraction
Smooth muscle contraction is a complex process vital for various bodily functions, from maintaining blood vessel tension to facilitating the movement of food through the digestive tract. Unlike striated muscles, smooth muscle contraction begins more slowly and lasts longer.
The onset of contraction is triggered by an increase in calcium ions within the sarcoplasm, similar to the process in striated muscle. However, smooth muscles have a relatively smaller reservoir of the sarcoplasmic...
The onset of contraction is triggered by an increase in calcium ions within the sarcoplasm, similar to the process in striated muscle. However, smooth muscles have a relatively smaller reservoir of the sarcoplasmic...
01:17Autoregulation of Blood Flow
Autoregulation mechanisms are characterized by their inherent capacity for self-regulation without necessitating specific nervous stimulation or endocrine control. These mechanisms facilitate the adjustment of blood flow and, therefore, perfusion specific to each tissue region. This self-regulation encompasses chemical signals and myogenic controls.
Chemical Signaling in Autoregulation
Chemical signaling operates at the precapillary sphincter level, inciting either contraction or relaxation.
Chemical Signaling in Autoregulation
Chemical signaling operates at the precapillary sphincter level, inciting either contraction or relaxation.
01:16Vascular Spasm
The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last for...