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BSc module 3 > Intro to the endothelium > Flashcards

Intro to the endothelium Flashcards

1
Q

How much of heart is endothelial cells?

A

3:1 Endotheliam:CM

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2
Q

Why don’t endothelial cells become 3D structure?

A

Contact inhibition

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3
Q

Key property of endothelial cells

A

quiescent

I.e. not actively proliferating (average lifespan of an EC > 1 year)

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4
Q

Size of endothelial cell

A

1-2 μm thick and ~ 10-20 μm in diameter

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5
Q

What are endothelial cells?

A

A single layer of flat cells that line the entire vascular system (blood and lymphatic vessels)

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6
Q

Yolk cells become…

vascular

A

Inner become primary plexus to form yolk vasculature

Outer become blood cells

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7
Q

Embryo proper becomes..

vascular

A

Primary plexus differentiates into more specialised endothelial cells associated with artery and vein
from cardinal vein - lymphatic endothelial cells

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8
Q

Where do hematopoietic stem cells (HSC) originate from

A

Endothelium
- Specialised endothelium: hemogenic endothelium
Different transcription factors switched on/of

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9
Q

Which transcription factor switched on for endothelial to HSC transition?

A

Runx 1

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10
Q

Which transcription factor switched off for endothelial to HSC transition

A

HoxA3

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11
Q

Key marker for HSC

A

Runx1

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12
Q

Crucial marker for lymphatic endothelial cells and why

A

Prox1 because not found in other endothelial cells

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13
Q

Applications of tissue engineering of blood vessels

A
  • Vascular graft for coronary and bypass surgery

- Vascular networks for organ regeneration

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14
Q

Endothelial cell heterogeneity

A

Not all EC in the body are the same: structural, functional, and genetic differences according to the position in the cardiovascular tree

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15
Q

Endothelial cell marker

A

(VWF, CD31, VE- Cadherin)

but there is no universal EC marker present exclusively in EC and in all EC

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16
Q

Permeability variations between endothelial cells

A

• Continuous, non-fenestrated: caveole system Tight junctions
• Continuous, fenestrated: discontinuous sinusoidal Found in filtration organs
Regulation of permeability, regulated by certain proteins
• Post capillary venules

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17
Q

Leucocyte trafficking

A

process is slightly different in

different types of endothelium and differing cell types → Stochastic switching of endothelial cells

18
Q

What do endothelial cells regulate?

A 
Permeability
Inflammation
Thrombosis and haemostasis
Vascular tone
Angiogenesis
Leukocte transmigration
19
Q

What do endothelial cells make?

A 
Matrix products, adhesion molecules, inflammatory mediators
Antithrombotic and procoagulant factors
Vasodilator and vasoconstricting factors
Growth factors
KEY IS BALANCE
20
Q

What is VE cadherin

A

Fundamental, cell-cell contract molecules

Ca2+ dependent adhesion molecule at endothelial adherens junctions

21
Q

Role of VE cadherin

A
  • Homophilic interaction with VE-Cadherin on opposite cells
    • Inside the cell, binds to catenins to mediate interaction with actin cytoskeleton and signalling
    • Regulates permeability, survival, shear stress and growth factors signals
22
Q

Pathway of functions for VE cadherin

A

Wnt/b-catenin signalling

23
Q

What modulates function of VE cadherin?

A

Phosphorylation

- disrupts junctions and and this increases permeability and leukocyte migration between endothelial cells

24
Q

Basic b-catenin signalling pathway

A
  1. Two cells in contact, following angiogenesis
  2. β catenin is sequestered away with VE cadherin at the organised adherens junction
    it is on the membrane and does not have an effect
  3. When required (or in pathology) β catenin comes off from where it is being inhibited
  4. Goes into the nucleus
  5. To become a transcriptional cofactor
    → proliferation survival
25
Q

VEGF control of endothelial haemostasis

A

Cell prolifertaion, survival, migration etc

26
Q

Important pathway for stability of endothelium and vasculature

A

Angiopoietin-Tie2 ligand-receptor system

27
Q

What is the Angiopoietin-Tie2 ligand-receptor system

A
  • Ang-1 and Ang-2 are antagonistic ligands of the Tie2 receptor
  • Ang-1 binding to Tie2 promotes vessel stability and inhibits inflammatory gene expression
  • Ang-2 antagonises Ang-1 signalling, promotes vascular instability and VEGF-dependent angiogenesis
28
Q

What is angiopoietin 1 synthesies by

A

pericytes found bound to vascular cells

29
Q

Role of angipoietin 1

A

Binds to TIE2 receptor

  • series of phosphorylation events
  • inhibits NKkB = Anti-inflammatory
  • activate pik3 = survival
  • inhibit leukocyte recruitment by downregulation of adhesion molecules
30
Q

Where does angiopoietin 2 come from

A

Weibel-palade bodies (formed from vWF) within endothelial cells

31
Q

What does angiopoietin 2 do

A

Released from endothelial cells by inflammatory stimuli

  • Antagonises binding of ang 1 to the TIE 2 receptor
    • opposite effect of Ang1 -
32
Q

Endothelial homeostasis

When is it diminished?

A

Inflammatory, proliferation, thrombotic
Balance of pro and anti factors
If there is constant activation of the endothelium E.g.. Constant inflammation stimulus, high LDL
The constant stimulation prevents the endothelium form switching back to the resting state and balance
Prolonged activation can be very detrimental

33
Q

Signals that switch endothelium into pro-inflammatory state and what does it lead to

A 
OxLDL
High BP
Smoking
Viruses
Mechanical stress
High glucose
Inflammation

Leads to ACTIVATION OF ENDOTHELIUM

34
Q

what does activation of endothelium lead to?

A

Thrombosis
Permeability
Leukocyte recruitment
Angiogenesis

–> ATHEROSCLEROSIS

35
Q

Pathogenesis of atherosclerosis

A

(1) Endothelial activation
Promotes increased permeability, leukocyte migration, etc.
(2) Leads to fatty streak formation Early lesion
Accumulation of fat and cholesterol
(3) Formation of an Advanced, Complicated Lesion of Atherosclerosis.

36
Q

Leukocyte recruitment in normal conditions

A

Recruitment of blood leukocytes into tissues takes place normally during inflammation: leukocyte adhere to the endothelium of post-capillary venules and transmigrate into tissues

37
Q

Leukocyte recruitment in atherosclerotic conditions

A

In atherosclerosis, leukocytes adhere to activated endothelium of large arteries and get stuck in the subendothelial space

38
Q

Physiological role of leukocytes

A

normal immune surveillance and inflammation

39
Q

Pathological role of leukocytes

A

Pathological role in chronic inflammatory diseases – atherosclerosis, rheumatoid arthritis, asthma, vasculitis, psoriasis
Recruitment of blood leukocytes into tissues takes place normally during inflammation: leukocyte adhere to the endothelium of post- capillary venules and transmigrate into tissues
• In atherosclerosis, leukocytes adhere to activated endothelium of large arteries and get stuck in the subendothelial space
• Newly formed post-capillary venules at the base of developing lesions provide a further portal for leukocyte entry

40
Q

Angiogenesis and CV disease paradox

A
  1. Promotes atherosclerotic plaque growth and rupture

2. Therapeutic angiogenesis induces new vessel formation in ischemic tissues

BSc module 3 (10 decks)

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