Endothelial cells Flashcards

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1
Q

What does the vascular network regulate?

A
  • molecule and cell movement
  • physiological responses by different organs
  • pathogenic infection and immune responses
  • disease states e.g. cancer, heart disease
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2
Q

What are disease states linked to endothelial dysfunction?

A
cancer
heart attacks
strokes
PAD
preeclampsia
Dementia
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3
Q

blood vessels?

A
Artery
Arteriole
Capillary
Venule 
Vein
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4
Q

What is the blood pressure in arteries, veins and capillaries?

A

arteries - 80-120 mm Hg
Vein - 30 mm Hg
Capillary 8-10 mm Hg

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5
Q

What is the structure of the capillary?

A

thin endothelial barrier between ECM and blood

fenestrations

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6
Q

What is endothelial heterogeneity?

A

input-output device
responds to both biochemical and mechanical changes
cells slightly different based on where they are

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7
Q

What is endothelial input-output activity?

A
  • cell adhesion
  • response to grwoth factors
  • interaction with migrating cells
  • balance between quiescence, proliferation and death
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8
Q

What are the key physiological features of endothelial cells?

A
  • vasculogenesis
  • angiogenesis
  • vascular homeostasis
  • blood clotting
  • disease related functions
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9
Q

What is the endothelial balancing act?

A

need to balance action as this effects ability to deal with major disease states

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10
Q

How is angiogenesis involved in cancer?

A

growth depends on it

metastasis via spread of tumour cells

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11
Q

How does hypoxia stimulate angiogenesis?

A

synthesis of pro-angiogenic factors

VEGF-A synthesis

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12
Q

What is angiogenesis dependent on?

A

HIF-1 activity
synthesis of VEGF-A - binds to cognate receptors

block interactions to treat cancer e.g. Avastin, Sutent

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13
Q

What is the oxygen-regulated HIF-1 switch?

A

availability of different sets of genes

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14
Q

What is the variety in VEGF receptors

A

RTKs
Non-RTKs
Non-RTK

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15
Q

What is involved in VEGFR of growth and survival?

A

confluent cell monolayer = survival response to VEGF-A

Sub-confluent cells = growth response to VEGF-A

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16
Q

What is endothelial sprout organsiation?

A

when VEGF hits a blood vessel = sprout

blood vessel sprout express DII4 ligands

Stalk cells express Notch and VEGFR2

17
Q

What are endothelial signalling pathways?

A

VEGFR2 signalling - positively regulates angiogenesis

Notch signalling negatively regulates angiogenesis

18
Q

What are endothelial-leukocyte interactions?

A

PECAM-1 - binding between endothelial cells and leukocytes

VCAM-1 - binds a4b1 integrin

help leukocyte roll and firmly adhere

19
Q

What is Trans-Endothelial Migration (TEM)

A

Diapedesis
leukocyte squeezes between 2 endothelial cells
leukocyte moves into the ECM layer
EC-EC connections have to be disrupted and reformed

20
Q

What is Atherosclerosis?

A
  • Plaques/lesions
  • Fat-filled streaks or lesions
  • Major artery blockage by blood clots
  • causes heart attacks/strokes
21
Q

How are endothelium-leukocyte interactions important in atherosclerosis?

A
  • monocytes bind to endothelium - differentiate into macrophages which bind modified LDLs
  • die and form lesions in vessel wall
22
Q

What is atherosclerotic Plaque Rupture?

A
damaged endothelium
Blood clot/thrombus
Increased blood pressure
arterial blockage 
clinical symptoms
23
Q

what is the role of NO?

A

vascular smooth muscle relaxation

blocks leukocyte adhesion

blocks platelet aggregation

24
Q

What is Endothelial Stem Cell Therapy?

A

isolation of EPCs
Differentiation in vitro to ECs
Re-implantation of differentiated cells into damaged tissue in vivo e.g. damaged heart or blood vessel tissues

25
Q

What is endothelial progenitor cell therapy?

A

isolation of EPCs
differentiation in vitro
Re-implantation into damaged tissue in vivo e.g. damaged heart

26
Q

What are endothelial derived tumours?

A

KSHV

  • linked to HIV
  • infects endothelial cells
  • Forms metastatic tumours
27
Q

What is KSHV-mediated endothelial transformation?

A

KSHV encoded gene mediates endothelial cell transformation
viral GPCR blocks cell death
elevates signalling and expression of growth factors

proliferate and behave like typical transformed cancer cell - express lytic genes that induce paracrine angiogenesis

also latent phenotype with transcriptional reprogramming