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Elastin is Responsible for Tissue Elasticity01:12

Elastin is Responsible for Tissue Elasticity

Elastic fiber contains the protein elastin along with lesser amounts of other proteins and glycoproteins. The main property of elastin is that it will return to its original shape after being stretched or compressed. Elastic fibers are prominent in elastic tissues found in skin and the elastic ligaments of the vertebral column.
Ligaments and tendons are made of dense regular connective tissue, but in ligaments not all fibers are parallel. Dense regular elastic tissue contains elastin fibers and...
Vascular Spasm01:16

Vascular 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...
Extracellular Matrix01:26

Extracellular Matrix

Unlike epithelial tissue, which is composed of cells closely packed with little or no extracellular space in between, connective tissue cells are dispersed in a matrix. This extracellular matrix (ECM) is composed of fibrous proteins like collagen, elastin, and fibronectin in a ground substance consisting of interstitial fluid, cell adhesion proteins, and proteoglycans. The proteoglycans form a gel-like material in the spaces between cells and provide hydration, buffering, binding, and force...
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...

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Related Experiment Video

Updated: Jun 5, 2026

Assessing Collagen and Elastin Pressure-dependent Microarchitectures in Live, Human Resistance Arteries by Label-free Fluorescence Microscopy
09:58

Assessing Collagen and Elastin Pressure-dependent Microarchitectures in Live, Human Resistance Arteries by Label-free Fluorescence Microscopy

Published on: April 9, 2018

Elastin and vascular disease.

M Keating1

  • 1Cardiology Division, Department of Human Genetics and Eccles Program in Human Molecular Biology and Genetics, University of Utah, Salt Lake City, UT 84112, USA.

Trends in Cardiovascular Medicine
|January 20, 2011
PubMed
Summary
This summary is machine-generated.

Supravalvular aortic stenosis (SVAS) is a genetic vascular disease affecting large arteries. Loss of vascular elasticity due to elastin gene mutations or deletions causes this condition, leading to obstruction.

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Last Updated: Jun 5, 2026

Assessing Collagen and Elastin Pressure-dependent Microarchitectures in Live, Human Resistance Arteries by Label-free Fluorescence Microscopy
09:58

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Mechanical Testing of Mouse Carotid Arteries: from Newborn to Adult

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Elastomeric PGS Scaffolds in Arterial Tissue Engineering
08:35

Elastomeric PGS Scaffolds in Arterial Tissue Engineering

Published on: April 8, 2011

Area of Science:

  • Cardiovascular Genetics
  • Vascular Biology
  • Medical Genetics

Background:

  • Supravalvular aortic stenosis (SVAS) is a vascular disease impacting major arteries like the aorta and pulmonary arteries.
  • It can be inherited as an autosomal dominant trait or occur within Williams syndrome.
  • Genetic factors, particularly involving the elastin gene, are implicated in SVAS development.

Purpose of the Study:

  • To investigate the genetic basis of Supravalvular aortic stenosis (SVAS).
  • To understand the molecular mechanisms linking elastin gene alterations to vascular obstruction.
  • To differentiate the genetic causes of isolated SVAS versus SVAS in Williams syndrome.

Main Methods:

  • Molecular genetic studies were employed to analyze elastin gene alleles.
  • Analysis focused on identifying mutations and deletions within the elastin gene.
  • Comparison of genetic findings in patients with isolated SVAS and Williams syndrome.

Main Results:

  • Mutations in a portion of an elastin allele were found to cause autosomal dominant SVAS.
  • Submicroscopic deletions disrupting the entire elastin gene are associated with Williams syndrome.
  • These findings highlight the role of elastin gene integrity in vascular health.

Conclusions:

  • Loss of vascular elasticity, stemming from elastin gene defects, is a key factor in vascular obstruction in SVAS.
  • Genetic alterations in the elastin gene are central to the pathogenesis of SVAS.
  • Understanding these genetic links provides insight into the broader mechanisms of vascular disease.