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Glossary/terms of all lectures Vascular Biology
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Lecture 1, 2 and 3: Introduction, current concept and endothelial dysfunction invascular pathology
Thrombosis Atheroma build-up can cause thrombosis and thrombosis can cause ischemia at the
site of occlusion
Cardiovascular risk factors These are factors that are capable of increasing the risk at cardiovascular diseases
Non-modifiable risk These are factors that are not adjustable. Examples are: age, gender/sex, genetic
factors factors, race and ethnicity
Modifiable risk factors Factors that we can adjust. Examples are: high BP,
The response to injury Toxic injury due to increased plasma lipoproteins being mainly oxLDL, resulting in
model endothelial denudation is the initiating event. There is toxic injury in your blood
plasma and results in endothelial denudation. This injury is then prone to
atherosclerosis
The lipid theory Diet with pure cholesterol results in fast development of atherosclerosis. After this
purification of the LDL receptor: if the LDL receptor is not functioning anymore, LDL
remains surface bound
Endothelial dysfunction Endothelial cells can be injured by modified LDL, hypertension, differences in shear
stress and infectious micro-organisms. Endothelial dysfunction occurs and shows
increased endothelial permeability to lipoproteins, expression of adhesion
molecules and release of growth factors
The inflammatory model Inflammatory components that are very important to atherosclerotic lesion
development as well. Cellular infiltration in the outer layer of the vessel wall occurs
Atherosclerosis It is a lipid driven chronic inflammatory condition that occurs in the context of
endothelial dysfunction
Atheroma A big core of intracellular lipids
Fibroatheroma Fibers on top of the plaque are formed
Fibers cap weakening Results in plaque rupture
Vulnerable plaque A lot of definitions: the underlying plaque having the potential
to become thrombogenic if exposed to the appropriate
triggering stimuli. Furthermore: a lesion composed of lipid-rich
core and an overlying cap rich in macrophages. Lipids and
inflammation are common among vulnerable plaques.
It has not ruptured yet with a large lipid pool, a lot of
inflammatory cells and a fibers cap that can easily break
Stable plaque This is a plaque in which the lesion area is almost identical to the
vulnerable plaque, but the components are different. We have a
small lipid lake and little inflammatory cells. The cap is really thick
and does not rupture so fast.
Plaque rupture Often about a plaque with a large lipid core, a thin fibers cap,
blocked luman by a thrombus and a ruptured cap.
Afx Indicates problems with your eyes – temporal blindness
Tia This indicates symptoms of a stroke, but the symptoms are fone within two days
,Plaque erosion Plaques that are more fibrous with a lot of
collagen and smooth muscles, less fat and
inflammatory cells are not always stable.
These plaques can also give rise to thrombus
formations. Matrix and collagen is exposed to
blood and this gives rise to thrombosis. A
thrombus without a rupture, is called erosion.
Erosion is often the case in females, while
rupture is often the case in males
Tunica intima Inner layer of the vessel, which is in direct contact with the blood. This is the
thinnest layer
Tunica media This is the muscular layer that is responsible for contraction of the vessel and for
structure, elasticity and vasoreactivity. This is the thickest layer
Tunica adventitia This is the perivascular side of the vascular wall and provides strength and an
anchor in the surrounding tissues. It is the outermost layer that consists of mostly
ECM, collagen and elastic fibers. It contains vaso vasorae, autonomic nerves,
fibroblasts and macrophages
Microenvironment This is the local environment where the artery or vein is at
Epigenetics Regulated by your gene set and mostly the progenitor endothelial cells that are
recruited from the bone marrow
Continuous capillaries Present in our venous system. Nicely closed and present in the skin, lung and the
heart. It is really a barrier
Fenestrated capillaries More holes in between the endothelial cells that allow passing of materials. For
example in the kidney to allow exchange of certain toxins
Sinusoidal capillaries Larger holes in between the endothelial cells. Are found in the liver, but also in the
spleen and in bone marrow. Serum proteins and blood is allowed to pass
Semi-permeable barrier of This depends on the blood pressure. On the arterial end, blood pressure is high and
endothelial cells osmotic pressure is low. On the venous end, blood pressure is low and osmotic
pressure is high – resulting in the exchange of materials
Glycocalyx It is a layer on the inner side of the vessel wall, on top of the endothelial layer. It is
made up out of porteoglycans and sugars to form a sort of additional barrier on the
inside of your vessel wall. Important during inflammation and homeostasis or
pathology. It is a biomechanical sensor
LPS A bacterial compound that highlights the fact that there might be an infection going
on and inflammatory cells need to come in
Disturbed flow Results in endothelial dysfunction. There is a
loss of the glycocalyx and the barrier function
is decreased. There is less eNOS which
normally it in shape
,eNOS Endothelial regulation of the
underlying vascular smooth
muscle cell goes via nitric
oxide (NO-). This is all
regulated by nitric oxide.
eNOS is reduced in healthy
endothelial cells and this can
be converted into NO. NO
induces contraction. When
this balance is off, we get eNOS uncoupling thereby causing ROS. This results in
desensitization to NO and smooth muscle cells can no longer respons to NO →
endothelial dysfunction
NFκB Master switcher of inflammation and activated after endothelial activation
Leukocyte rolling Leukocyte binds to activated endothelial cell and starts to roll. If there is an
upregulation of adhesion molecules, the leukocyte will firmly adhere to the
endothelial layer to eventually migrate into the tissue
Haemostasis and Healthy endothelium had anti-thrombotic and anti-coagulatory functions.
coagulation
NO- Prevents thrombosis by preventing coagulaton factors to occur
PGI2 (prostacyclin) Prevents thrombosis by preventing coagulaton factors to occur
fibrinolysis Cleaving fibrin into smaller components
Tipp cells This is the endothelial cell that actually moves the whole process of angiogensis
Endothelial cell This is caused by aging or by disease. This is also present in atherosclerosis. The
senescence endothelial cells have a more flattened and enlarged morphology and are relatively
resistant to apoptosis. More production of pro-inflammatory factors are present
EndoMT Endothelial to Mesenchymal transition
is a mechanism when we talk about the
plasticity of cells. In vitro this is done
by exposing endothelial cells to TGFβ
and extra inflammatory cytokins like
TNF and they start to change shape.
First there are a lot of endothelial like
marker and after transition a lot of
smooth muscle cell marker occur
Lecture 4: Cellular movement
Chemotaxis This is the directed movement of cells
fMLP A bacterial compound forming a gradient for neutrophils. The neutrophils move
towards this compound
Chemoattractant Towards the site of inflammation
Chemorepellent Pushes the cell away
Rolling Leukocyte is rolling because they bind to adhesion molecules with a low affinity.
Endothelial cells become activated to slow the rolling and to arrest the cell.
Chemokines are responsible for this. ICAM and PECAM are involved in intravascular
crawling. Transcellular migration occurs
ICAM Adhesion molecule endothelium
PECAM Adhesion molecule endothelium
Chemokines Compound that are responsible for attracting leukocytes towards the inflammatory
site
Chemokine gradient The gradient helps cells to decide where to go and this gradient is very local around
the atherosclerotic plaque
C chemokines One cysteine residue
CC chemokines Two cysteine residues binding to each other
, CXC chemokines Have a carbon structure in between the cysteines
CX3C chemokines The red one!
Classical monocytes Often referred to as pro-inflammatory monocytes and binds strongly to CCR2 and
very weak to CX3CR1
Intermediate monocytes Bind strongly to CX3CR1 and very weak to CCR2
Non-classical monocytes Bind strongly to CX3CR1 and very weak to CCR2
M1 macrophages Derived from the classical monocyte. Pro-inflammatory macrophages that produce
a lot of pro-inflammatory cytokines and different interleukins. On inflammatory
conditions they are involved in bacterial clearance and proteolysis. In the
atherosclerotic plaque they are involved in foam cell formation
M2 macrophages We call this alternative. This is the anti-inflammatory macrophage which is involved
in tissue remodeling. They express different types of interleukins like IL-10 which is
one of the most well known anti-inflammatory IL. It is also involved in efferocytosis
which is the clearance of red blood cells and prevents atherosclerosis
MCP-1 Monocyte chemoattractant protein 1. This is very capable in recruiting monocytes
CCL2 This is the chemokine name of MCP-1 and is the strongest binder to CCR2. It is
produced both by endothelial cells and smooth muscle cells (and by endothelial
cells in atherosclerotic plaques)
CCR2 Receptor for CCL2 (MCP-1)
CCR2 KO The amount of cells that infiltrate in the peritoneal cavity is released when there is
no CCR2 present on the cells. Cell migration is not present
CX3CR1 This is a chemokine receptor as well. When there is no CX3CR1, we have less lesion
formation
CCL3 CCL3 levels are downregulated over time, but those patients experiencing a
secondary ACS had the highest level of CCL3 at admission. This suggests that this
chemokine might be useful to create a secondary plaque
CCL3, CCL5 and CCL18 Elevated levels of these chemokines combined, strongly predict future (fatal_
events
MCP1-7ND This is competitive receptor antagonist of the CCR2 receptor. This antagonist causes
a decreased lesion formation
MCN1202 Treatment with this decreases CRP levels in atherosclerotic patients. You see a
really reduced inflammation
Maraviroc Drug that decreased inflammatory proteins as CRP and also decreased IL-6
Lecture 5: Immune cells in atherosclerosis
Advanced plaque large necrotic core, a
lot of dead cell
material, cholesterol
remnants,
endothelial lining, a
layer of smooth
muscle cells to form
a small fibers cap.
Also a lot of
inflammatory cells
are included.
Classical humoral response Uptake of an antigen by an APC. Antigen presented on the class II MHC molecule to
a CD4 T cell which becomes activated. The T helper cell activates the B cells. The B
cells start to produce antibodies
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