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Printable Handouts
Navigable Slide Index
- Introduction
- Blood vessel wall
- Early atherosclerosis
- Atherosclerotic plaque
- Sites of vascular calcification
- Vascular calcification is a regulated process (1)
- Vascular calcification is a regulated process (2)
- Vascular calcification is regulated in vivo (1)
- Vascular calcification is regulated in vivo (2)
- Development of bone and vascular calcification
- Inhibitors and triggers of calcification
- Human vascular calcification in vitro
- Effect of extracellular Ca on mineral deposition
- Detection of apoptosis in nodules
- Effect of anti-Fas IgM on VSMC calcification
- Effect of ZVAD on VSMC calcification
- VSMC apoptotic bodies concentrate calcium
- Apoptosis initiates calcification
- Matrix vesicles initiate calcification
- Matrix Gla protein
- The activity of matrix Gla protein
- Gla and Ser domains effect VSMC calcification
- Do mineral deposits have biological activity?
- Large calcium crystals and human VSMCs
- Nano and microcrystals
- Effects of crystals on human VSMC viability (1)
- Effects of crystals on human VSMC viability (2)
- Bafilomycin A and crystal-induced calcium signals
- Mechanism of CaP crystal induced increase in Ca
- Conclusions
- Acknowledgements
- References and further reading
Topics Covered
- Overview of the blood vessel wall
- Atherosclerosis
- The regulation of Vascular Calcification, including in vivo models
- Inhibitors and triggers of Calcification
- In vitro models of vascular calcification
- The role of apoptosis in calcification
- The role of matrix vesicles in calcification
- How do mineral deposits affect cells in the blood vessel wall?
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Talk Citation
Proudfoot, D. (2014, February 4). Vascular calcification location, formation and biological activity [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 30, 2024, from https://doi.org/10.69645/TCKY8832.Export Citation (RIS)
Publication History
Financial Disclosures
- Dr. Diane Proudfoot has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
A selection of talks on Cardiovascular & Metabolic
Transcript
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0:00
My name is Diane Proudfoot.
I work at the Babraham Institute in Cambridge.
And I'm going to talk to you
about vascular calcification.
I'm going to talk about where it's located,
how vascular calcification is
formed and how it's regulated.
And I'm also going to talk about the biological activity of vascular calcification.
0:21
I would like to start by describing the normal structure of a blood vessel wall.
And this is a cartoon
image of a cross section
through a blood vessel wall.
You can see that the blood vessel
is made up of three distinct layers.
These are called the intima, the media, and the adventitia.
The layer that's exposed to the blood is called the intima.
And this is covered on the lumenal side
by a single sheet of endothelial cells.
The intima provides a smooth,
non-thrombogenic surface and acts
as a permeability barrier
to cells and macromolecules.
Beneath the intima is a sheet of elastic fibers.
And this is called the internal elastic lamina.
The layer below is called the media.
And this contains vascular smooth
muscle cells and matrix proteins.
The main function of smooth muscle cells
is to contract and to dilate to achieve normal vascular tone.
The outermost layer is the adventitia.
And this is separated from the media
by the external elastic lamina.
The adventitia layer contains fibroblasts, small blood vessels,
and it also contains nerve
innervation to the blood vessel.
1:34
In early atherosclerosis, some changes
occur in the intima layer of the blood vessel wall.
Endothelial cells become
activated or damaged.
And this causes the attraction
of leukocytes from the blood
to roll along the endothelium and to enter into the intima layer.
When inflammatory cells, such as macrophages, enter into the intima,
they secrete factors, proteins, and
chemo attractants, which attracts
smooth muscle cells from the media layer
to change their phenotype from
contractile to a secretory
phenotype or a repair phenotype in the intima of the blood vessel wall.
Another change that happens is that
lipid proteins from the blood
accumulate in the intima layer.
And also, at this very early stage,
you can start to detect some small
diffuse particles of calcium
phosphate crystals, which is
an early sign of calcification.