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Biochem exam 2 > Angiogenesis: role of VEGF and Hypoxia (Part 1 & 2) > Flashcards

Angiogenesis: role of VEGF and Hypoxia (Part 1 & 2) Flashcards

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1
Q

What is vasculogenesis?

A

embryonic formation of endothelial cells from mesoderm that form new blood vessels in blood islands
-give rise to heart and first primitive vascular plexus inside the embryo

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2
Q

What is angiogenesis?

A

needed to fully form the vascular network
-process by which new blood vessels form from pre-existing vessels formed in vasculogenesis

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3
Q

what is inside the angiogenetic cluster?

A

blood cells

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4
Q

Where are the first blood islands?

A

in the yolk sac

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5
Q

What is sprouting angiogenesis?

A

when tissues that have low nutrient and oxygen supply produce VEGF-A and induce endothelial cells to secrete proteases that degrade basement membrane and allow endothelial cells to escape original blood vessels
-form sprouts to neighboring cells
-extend toward the source of angiogenic signal (VEGF-A)

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6
Q

What does VEGF do in sprouting angiogenesis?

A

induce the secretion of proteases that will degrade basement membrane and allow endothelial cells to escape their original vessel walls
-they will proliferate and form sprouts connecting neighboring vessels

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7
Q

What is intussusceptive (splitting) angiogenesis?

A

formation of new blood vessels by splitting of preexisting vessel into two

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8
Q

Does angiogenesis continue after birth?

A

yes, it happens every month with periods and happens when you are healing wounds

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9
Q

What is the tunica interna?

A

endothelial cells that line arteries and veins

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10
Q

What is the tunica media?

A

layer of smooth muscle in arteries and veins

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11
Q

What is the tunica externa?

A

outside layer of arteries and veins made of elastin and collagen

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12
Q

Is smooth muscle layer thicker in veins or arteries?

A

arteries

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13
Q

What are capillaries made of?

A

only endothelial cells
-no muscle or elastin & collagen

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14
Q

What are pericytes?

A

support cells that wrap around capillaries that regulate permeability of capillaries they surround

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15
Q

What are the three types of capillaries?

A

continuous
fenestrated
sinusoid

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16
Q

continuous capillary

A

basement membrane is continuous (would be in blood brain barrier)

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17
Q

fenestrated capillary

A

has fenestrations on the endothelial layer

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18
Q

sinusoid capillary

A

incomplete basement membrane & intercellular gaps on endothelial layer (liver-areas w/ lots of blood flow)

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19
Q

What determines the type of capillary that is present?

A

the tissue type and the amount of interaction with blood

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20
Q

Growth factors in vasculogenesis:

A

VEGF and FGF

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21
Q

Growth factors in mature vessels:

A

Ang1 (stabilize blood vessel)

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22
Q

Growth factors in angiogenesis:

A

VEGF

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23
Q

Growth factors in mature circulatory system:

A

PDGF and TGF-b

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24
Q

Is VEGF a required angiogenic growth factor?

A

yes

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25
Is blocking VEGF lethal?
yes
26
is blocking 50% of VEGF lethal?
yes
27
Major form of VEGF and its receptor:
VEGF-A and VEGFR2 -involved in both vasculogenesis and angiogenesis
28
are there different forms of VEGF and its receptor?
yes- do not need to know specifics
29
What is the tip cell?
the end of the sprouting capillary that is seeking out VEGF
30
What is the cell that forms the tube of the sprouting capillary?
stalk cell
31
What induces sprouting angiogenesis?
hypoxia
32
What is present during hypoxic states that stimulates the start of sprouting angiogenesis?
hypoxia inducible factor (HIF)
33
What does HIF do?
cause cell to release VEGF
34
Why does HIF induce sprouting angiogenesis?
causes the capillaries to sprout towards the part that does not have enough oxygen -creates capillary interactions that bring oxygen to those spots that are lacking
35
What occurs to HIF during normoxia conditions?
HIF-a is hydroxylated and does not bind to HIF-b -HIF-a binds to pVHL -HIF-a gets ubiquitinated -go to proteasome for degradation
36
What occurs to HIF during hypoxic conditions?
HIF-a transported to nucleus where it binds to HIF-b -binds to DNA and causes release of VEGF
37
What inhibits Tie-2?
Ang-2 -allows for VEGF-A induced cell migration & division
38
What supports Tie-2?
Ang-1 -in stable blood vessels (normoxia conditions)
39
What does angiogenesis require of capillaries?
destabilization -allow for more growing and migration
40
What are the two oxygen sensing domains of HIF-1a?
PHD2 and FIH -oxygenated and tag for degradation (PHD2) or inactivation (FIH) -work at different levels of oxygen (lose PHD2 first-slightly hypoxic)
41
What is N-TAD involved with?
blocking the oxygenation of PHD
42
What is C-TAD involved with?
blocking both PHD and FIH
43
What does Ang-1 promote?
vessel maturation by stimulating migration, adhesion, and survival of endothelial cells *stability
44
What does Ang-2 promote?
disruption of connections between endothelium and perivascular cells
45
When Ang-2 and VEGF work together, what happens?
neovascularization
46
What does Ang-2 say to Ang-1?
hey get outta here
47
Where is Ang-1 usually made?
pericytes
48
Where is Ang-2 usually made?
endothelial cells
49
When Ang1 and Tie2 associate, what is occurring ?
the cell is maintaining integrity and quiescence
50
Where is ang-2 stored in endothelial cells?
Weibel-Palade bodies
51
what causes Ang-2 to be released from WPB?
inflammatory stimulus
52
where is Ang-2 normally expressed?
in the tip cells of angiogenic sprouts
53
What is PDGF?
released from tip cell and stimulates proliferation of the pericyte cells and smooth muscle cells
54
are vasculogenesis & angiogenesis required for healing of bone?
yes
55
Outline endochondral bone formation:
-start with just capillaries -cartilage forms from hypertrophic chondrocytes -blood vessels form in between the hypertrophic chondrocytes -attract osteoblasts and form bone that eventually replace the cartilage
56
Steps of bone regrowth following fracture:
-hematoma (day 0-5) -soft unmineralized cartilage (5-10) -fibrous tissue (10-16) -hard callus/ secondary bone (16-21) -hard callus/ remodeled bone (21-35)
57
What does Fit-IgG do?
inhibit VEGF from working in broken bone
58
Does osteoporosis speed up or slow down fracture healing?
slow down
59
What are hemangiomas?
benign proliferative lesions that are localized growths of capillary endothelium -up to 10% of all babies -caused by mutation in TEM8 or VEGFR2 genes
60
How do tumors become vascularized?
the tumor cells release VEGF which bind to VEGFR and cause capillaries to move towards them
61
What do endostatin and angiostatin do?
decrease proliferation and migration and increase apoptosis in endothelial cells also decrease the release of VEGF from tumor cells -inhibit angiogenesis
62
What is endostatin?
anti-angiogenic agent -naturally occurring C-terminal fragment of type 18 collagen
63
What is angiostatin?
38 kDa fragment of plasmin
64
Why are anti-angiogenic treatments used in cancer?
designed to prevent the formation of new blood vessels to tumors -do not completely eradicate -would need combination of drugs
65
How does bevacizumab work?
it is a monoclonal antibody that binds to VEGF and does not allow interaction with VEGFR
66
What is a type of anti-angiogenic drug that is in clinical development?
tyrosine kinase inhibitors
67
Where do type 1 tyrosine kinase inhibitors bind?
-bind in ATP binding cleft (active site)
68
Where do type 2 tyrosine kinase inhibitors bind?
hydrophobic region adjacent to ATP binding cleft -steric inhibition
69
What is macular degeneration?
chronic eye disease that causes vision loss in the center of your field of vision
70
Using VEGF inhibition does what to tumors ?
decreasing vascular supply and will cause tumor to decrease in size
71
VEGFA and VEGFR2 are involved in...
vasculargenesis and angiogenesis

Biochem exam 2 (9 decks)

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