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Biochem > Angiogenesis Role of VEGF and Hypoxia > Flashcards

Angiogenesis Role of VEGF and Hypoxia Flashcards

1
Q

what is vasculogenesis

A

de novo formation of blood vessels when there are no existing ones in the vicinity

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2
Q

what often pairs with vasculogenesis and why

A

angiogenesis, it is needed to fully form the vascular network

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3
Q

what does vasculogenesis give rise to in the fetus

A

the heart and the first primitive vascular plexus and its surrounding membranes

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4
Q

what happens in vasculogenesis

A

angiogenic cell clusters form blood islands in the yolk sac and these clusters give rise to red blood cells

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5
Q

what are the 2 sites that the vascular system forms in the embyro

A

the blood island of the yolk sac and one in the embryo proper

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6
Q

what is angiogeneis

A

the process by which new blood vessels form from pre-existing vessels that are formed in the early stages of vasculogenesis

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7
Q

what are the 2 types of angiogenesis

A

sprouting angiogenesis and intussusceptive angiogenesis

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8
Q

what is sprouting angiogenesis

A

tissues that have low nutrient and oxygen supply produce signals (VEGF-A) that induces endothelial cells to secrete proteases that degreade their BM and allow the endothelial cells to escape their original vessel walls. the cells proliferate and form sprouts connecting to neighboring vessels. extend towards the source of the angiogenic signal

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9
Q

what is intussusceptive angiogenesis

A

also known as splitting angiogenesis and is the formation of new vessels by splitting a pre-existing vessel in 2
- allows for increase in number of capillaries without an increase in endothelial cells

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10
Q

where does angiogenesis take place in adults

A

-in women when the lining of the uterus is shed during the menstrual cycle new blood vessels are formed
- wound repair

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11
Q

what is in the interior of the blood vessel

A

single layer of endothelial cells attached to and separated from the outer layers by the basal lamina

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12
Q

what makes up the blood vessel

A

loose CT outer layer, smooth muscle middle layer, and endothelial cells

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13
Q

what are the largest blood vessels? smallest?

A

largest- arteries and veins
smallest- capillaries and sinusoids

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14
Q

what do capillaries and sinusoids consist of?

A

endothelial cells and a basal lamina with scattered pericytes

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15
Q

what are pericytes

A

members of CT family, related to vascular SM cells that wrap themselves around the small vessels

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16
Q

what is the difference between arteries and veins

A
  • veins have a larger lumen
  • veins have a thinner external and middle layer
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17
Q

what makes up the wall of a capillary

A

a single layer of endothelial cells

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18
Q

what are the 3 types of capillaries

A

continuous, fenestrated and sinusoid

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19
Q

describe a continuous capillary

A

-solid synctitium of endothelial cells joined by junctions

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20
Q

describe a fenestrated capillary

A

have holes in the endothelial cells where material can move back and forth

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21
Q

describe a sinusoid capillary

A

gaps between endothelial cells and the basement membrane

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22
Q

what is pO2

A

a measure of how much O2 is dissolved in the blood

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23
Q

how many molecules of O2 can hemoglobin bind

A

4

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24
Q

what does BPG do to hemoglobin

A

decreases O2 affinity, O2 moves from Hb into plasma and into tissue

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25
Q

what would a right shift in hemoglobin affinity of O2 be caused by

A

-increased H+
-increased BPG
- increase temperature
- increased altitude

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26
Q

what would a left shift in hemoglobin affinity for O2 be caused by

A
  • decreased H+
  • decreased BPG
  • decreased temperature
  • decreased HbF
  • decreased CO
  • decreased MetHb
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27
Q

what does the oxygen binding/dissociated plot for hemoglobin say

A

beyond 95% saturation, Hb will dissolve O2

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28
Q

what paracrine factors are used in vasculogenesis and what do they give rise to

A

FGF2- mesoderm cells
VEGF- hemangioblasts which form tubes

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29
Q

what does ANG1 bind to and what happens

A

binds to tie-2 on the endothelial cell of the pericyte and maintains vessel integrity and quiescence

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30
Q

what is the paracrine factor in angiogenesis

A

VEGF

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31
Q

what does VEGF in angiogenesis do

A

produces a juvenile vascular system by sprouting and splitting

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32
Q

what paracrine factors does the mature circulatory system use

A

PDGF and TGFbeta

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33
Q

what do PDGF and TGFbeta do

A

maturation and remodeling to produce a mature vascular system

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34
Q

what do antibodies against VEGF block

A

embyronic development
- bone morphogenesis
- female reproductive cycling
- corneal angiogenesis
- growth of several tumor types in animal models

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35
Q

what happens when VEGF is blockes in embryonic development

A

it is legal even a 50% reduction

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36
Q

what type of receptors are VEGF receptors

A

tyrosine kinase receptors

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37
Q

what does VEGF-A bind to and what does it regulate

A

binds to VEGFR-1 and VEGFR-2 and regulates vasculogenesis, angiogenesis, inflammatory responses, and carcinogenesis

38
Q

what does VEGFR-1 modulate

A

placenta and macrophages and vasculogenesis and angiogensis

39
Q

what does VEGFR-2 modulate

A

vasculogenesis and angiogenesis

40
Q

what does VEGFR-3 modulate

A

lymphangiogenesis

41
Q

what do pseudopodial processes do

A

guide the development of the capillary sprout as it grows into the surrounding tissue

42
Q

what happens with angiogenesis when O2 levels are low

A

results in high HIF which induces cells to secrete VEGF. VEGF then stimulates capillary sprouting and angiogenesis

43
Q

what happens with angiogenesis when O2 levels are high

A

HIF is low so not VEGF gets secreted for angiogenesis

44
Q

what senses O2 levels

A

HIF (hypoxia induced factor)

45
Q

what regulates HIF-1

A

pVHL- von hippel lindau tumor suppressor

46
Q

what happens with HIF mechanistically with hypoxia

A

moves into the nucleus to express VEGF to stimulate angiogenesis

47
Q

what happens with HIF mechanistically with normoxia

A

O2 hydroxylates HIF-1alpha then binds to a pVHL which degrades HIF-1 by ubiquidination

48
Q

what enzyme catalyzes the degradation of HIF-1alpha in normoxia

A

prolyl hydroxylases

49
Q

what 3 levels is VEGF-A expression controlled at

A

transcription, messenger RNA, stability, and translation

50
Q

what angiogenic factors are induced by hypoxia

A

VEGF-A and Ang-2

51
Q

what happens when VEGF-A and Ang-2 bind in hypoxia

A

Tie-2 and VEGFR2 are recruited and this leads to sprouting angiogenesis

52
Q

what happens with ANG-1

A

Tie-2 is signaled which activates a notch pathway which results in quiescence of the endothelial cell (nothing happens)

53
Q

what inhibits ANG-1

A

ANG-2

54
Q

what do HIF prolyl hydroxylase and HIF asparaginyl-hydroxylase do

A

they lead to inactivation and protosomal degradation of both domains of HIF-1alpha

55
Q

what portion of genes of HIF-1alpha are activated with low hypoxia

A

the N-TAD genes
(amino terminal activation domain)

56
Q

what portion of genes of HIF- 1 alpha are activated with high hypoxia

A

the N-TAD genes and the C-TAD genes (carboxy-terminal activation domain)

57
Q

what does ANG-1 promote

A

vessel maturation by stimulating migration adhesion and survival of endothelial cells

58
Q

what does ANG 2 do

A

-depends on if VEGF is present
- antagonist of Ang-1 and blocks its ability to bind to Tie-2 receptor
- disrupts connections between the endothelium and perivascular cells
- with VEGF ANG-2 promotes neo-vascularization

59
Q

what releases ANG-1

A

pericytes

60
Q

what does binding of ANG-1 to Tie-2 do

A

promotes vessel integrity, inhibits vascular leakage and suppresses inflammatory gene expression, stabilizing tight junctions in endothelial cells

61
Q

when is ANG-2 released and what is it stored in

A

during hypoxia, stored in weibel palade bodies

62
Q

what does ANG-1 do

A

promotes quiesence and stability of vessels

63
Q

what does ANG-2 do

A

stimulates sprouting

64
Q

what do tip cells do

A

get induced by ANG-2 to start the migration process

65
Q

what part of the cell do ANG-2 and VEGF act on

A

the tip

66
Q

how does PDGF stimulate proliferation of pericytes and smooth muscle cells

A

PDGF is synthesized and secreted by tip cells. PDGF binds to HSPG which makes pericytes come in and bind to endothelial cell layer and surround the vessel

67
Q

what happens in endochondral bone formation

A

-mesenchymal cells lay down avascular cartilage
-these differentiate into hypertrophic chondrocytes which signal to vascularize the forming bone
- then you get long bone with different layers of chondrocytes with bone marrow and vascularization

68
Q

what are the stages of bone fracture repair

A

hematoma ->soft callus -> fibrous tissue ->hard callus -> remodeling

69
Q

how does fracture repair involve VEGF

A

it is required for repair

70
Q

how is fracture healing impaired in osteoporosis

A

it takes longer and doesnt heal as well

71
Q

what is a hemangioma

A

benign highly proliferative lesions involving abberant localized growth of capillary endothelium . caused by TEM8 or VEGFR2 genes. benign

72
Q

what happens as tumors grow

A

they produce large quantities of VEGF

73
Q

what does VEGF recuit in tumors

A

lymphatics and angiogenesis factors to create own blood supply, ANG1 ANG2, and TDGF

74
Q

what is the environment of tumors and what does this recuit

A

hypoxic, recruits HIF 1 alpha

75
Q

what are the naturally occuring inhibitors of angiogenesis

A

endostatin and angiostatin

76
Q

what do endostatin and angiostatin do when they bind to endothelial cells

A

promote apoptosis and inhibit proliferation and migration

77
Q

what do endostatin and angiostatin do when they bind to tumor cells

A

down regulate VEGF

78
Q

what is endostatin dervied from

A

type 18 collagen

79
Q

how is endostatin released

A

from the breakdown of type 18 collagen

80
Q

what is angiostatin derived from

A

plasmin (derived from plasminogen) that gets broken down into kringle fragments

81
Q

what are angiogenesis inhibitors designed to prevent

A

formatino of new blood vessels which stops growth and spread of tumors

82
Q

how is endostatin treatment effective

A

in doses until tumor doesnt grow

83
Q

what is the mechanism of some anti-cancer angiogenesis inhibitors

A

they eliminate the activity of a binding domain so when the ligand binds, nothing happens. tyrosine kinase inhibitors

84
Q

what is macular degeneration

A

chronic eye disease that causes vision loss in the center of your field of vision. caused by deterioration of the macula

85
Q

where do tumors grow in the eye

A

iris because it is highly vascularized

86
Q

what does PGI2 do

A

inhibits platelet activation and is an effective vasodilator

87
Q

what does eNOS do

A

generates NO in the vascular endothelium, rates vascular tone, cellular proliferation, leukocyte adhesion, and platelet aggregation

88
Q

what does NO do

A

powerful vasodilator with a short half life, intercellular messenger that relaxes smooth muscle

89
Q

what do endothelins do

A

constrict blood vessels and raise BP

90
Q

where are VEGF receptors found

A

on the membrane

Biochem (34 decks)

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