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Applied Biochemistry > Angiogenesis: Role of VEGF and Hypoxia > Flashcards

Angiogenesis: Role of VEGF and Hypoxia Flashcards

1
Q

vasculogenesis

A

the embryonic formation of endothelial cells from the mesoderm layer precursors to form new blood vessels in blood islands

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2
Q

vasculogenesis is often paired with

A

angiogenesis

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3
Q

angiogenesis is needed to fully form

A

the vascular network

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4
Q

vasculogenesis gives rise to (2)

A

the heart and the first primitive vascular plexus inside the embryo and in its surrounding membranes

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5
Q

where does the vascular system form in the embryo? (2)

A

blood islands of the yolk sac

embryo proper

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6
Q

angiogenesis

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

two types of angiogenesis

A

sprouting angiogenesis

intussusceptive angiogenesis

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8
Q

sprouting angiogenesis

A

tissues that have low nutrient and oxygen supply will produce signals (VEGF-A) that induces endothelial cells to secrete proteases that degrade their basement membranes and allow the endothelial cells to escape their original vessel walls. These cells continue to proliferate and form sprouts connecting neighboring vessels, guided by extending towards the source of the angiogenic signal

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9
Q

intussusceptive angiogenesis

A

also known as splitting angiogenesis is the formation of new vessels by splitting a pre-existing vessel in two

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10
Q

example of angiogenesis in women

A

menstruation, each month for a few days in the lining of the uterus during the menstrual cycle as new blood vessels are formed

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11
Q

another example of angiogenesis

A

would repair

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12
Q

The largest of the blood vessels are the (2)

A

arteries and veins

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13
Q

arteries and veins have a tough, thick layer of (2)

A

connective tissue and many smooth muscle cells

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14
Q

The thickness of these layers varies depending upon the (2)

A

diameter and function of the vessel

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15
Q

The interior of the blood vessel consists of

A

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

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16
Q

The finest branches of the vasculature are the (2)

A

capillaries and sinusoids

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17
Q

These consist of only (3)

A

endothelial cells and a basal lamina together with a few scattered pericytes

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18
Q

These cells are members of the connective-tissue family, related to

A

vascular smooth muscle cells

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19
Q

Pericytes wrap themselves around

A

the small vessels and have other important functions

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20
Q

capillaries are very thin, composed of

A

a single layer of endothelial cells

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21
Q

what is the main role of circulation?

A

supplying oxygen to tissues

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22
Q

pO2 is a measure of

A

how much O2 is dissolved in the blood

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23
Q

hemoglobin contained in RBCs can bind up to

A

4 molecules of O2

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24
Q

neutralizing antibodies against VEGF block (5)

A 
embryonic development 
bone morphogenesis 
females reproductive cycling 
corneal angiogenesis 
growth of several tumor types in animal models
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25
Q

VEGF is required for

A

embryonic development

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26
Q

blocking VEGF is

A

lethal

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27
Q

even a 50% reduction of VEGF is

A

lethal

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28
Q

VEGF is required for

A

developmental angiogenesis

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29
Q

what type of receptors are VEGF receptors are

A

tyrosine kinase receptors

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30
Q

VEGF-a

A

a major contributor to angiogenesis, bind and activates VEGFR1 and VEGF2 and regulates vasculogenesis, angiogenesis, inflammatory responses, and carcinogenesis

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31
Q

The soluble form of VEGFR-1 appears to be an important modulator for the

A

placental vasculature

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32
Q

VEGF-C and -D mainly activate VEGFR-3 and regulate

A

lymphangiogenesis

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33
Q

The extracellular domain of VEGFR-3 is once cleaved and joined with

A

disulfide bond

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34
Q

pseudopodial processes guide the development of the

A

capillary spout as it grows into the surrounding tissue

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35
Q

hypoxia induces

A

spouting angiogenesis

36
Q

when oxygen concentration drops, this acts as a stimulus trigger to induce the transcription and secretion of

A

VEGF by the hypoxic cells

37
Q

VEGF then acts to stimulate

A

capillary sprouting and angiogenesis, reversing the hypoxia

38
Q

VEGF-a expression is controlled at which three levels?

A

transcription
mRNA stability
translation

39
Q

ang-1 promotes vessel maturation by stimulating (3)

A

migration, adhesion, and survival of endothelial cells

40
Q

ang-2 has different effects depending upon whether

A

VEGF is present or not

41
Q

importantly, ang-2 is an antagonist of

A

ang-1 and blocks its ability to bind to the tie-2-receptor

42
Q

ang-2 disrupts connections between the

A

endothelium and perivascular cells

43
Q

in combination with VEGF, ang-2 promotes

A

neo-vascularization

44
Q

PDGF stimulates proliferation of

A

pericytes and smooth muscle cells

45
Q

what is absolutely required for successful fracture healing of bone?

A

vasculogenesis/angiogenesis

46
Q

endochondral bone formation mechanism

A

condensation of mesenchymal cells which form cartilage in the presence of a vascular bed. form hypertrophic chondrocytes which put down a cartilaginous matrix that turns into bone

47
Q

femur fracture repair

A

initially forms a hematoma
soft callus/unmineralized cartilage is deposited by chondrocytes
vascular angiogenesis forms fibrous tissue
cartilage is replaced with new bone to form hard callus/secondary bone
hard callus/remodeled bone

48
Q

healing in younger individuals is quicker than

A

healing in older individuals

49
Q

fracture healing requires

A

VEGF

50
Q

fracture healing in osteoporotic bone vs normal bone

A

healing is delayed significantly, bone doesn’t achieve the same level of mechanical stability as normal individuals. this is a contributor to morbidity/fatality associated with osteoporosis

51
Q

hemangioma, hereditary capillary

A

begins highly proliferative lesions involving aberrant localized growth of capillary endothelium. they are the most common tumor in infancy occurring in up to 10% of all babies

52
Q

hemangioma is caused by

A

a gremlin mutation in TEM8 (a tumor specific endothelial cell marker) or VEGFR2 genes

53
Q

hallmark of tumor development

A

angiogenesis

(tumors need independent blood supply as they grow so they secrete VEGF and other growth factors for angiogenesis

54
Q

3 essential ways that VEGF may affect tumor vasculature?

A

?

55
Q

VEGFR1
VEGFR2
VEGFR3

A

1: stalk of endothelium
2: stalk of endothelium
3: lymphatic endothelial cell

56
Q

what happens when tumor cells secrete VEGF?

A

cancer cell secretes VEGF, binds to receptor, initiates relay proteins/intracellular 2nd messengers which stimulate new endothelial growth or stimulate growth of the tumor itself

57
Q

endostatin and angiostatin target

A

endothelial and tumor cells

58
Q

endostatin and angiostatin lead to

A

inhibition of angiogenesis

59
Q

how is angiogenesis inhibited by endostatin and angiostatin? (2)

A

down regulate proliferation migration
upregulate apoptosis
down regulation of VEGF

60
Q

problem with endostatin and angiostatin

A

they’re not specific to the tumor cells, so they may have consequences such as stopping angiogenesis where/when we need it

61
Q

endostatin

A

naturally occurring, 20 kDa C-terminal fragment derived from type 18 collagen

62
Q

endostatin is reported to serve as an

A

anti-angiogenic agent, similar to angiostatin and thrombospondin

63
Q

angiostatin

A

38 kDa fragment of a larger protein, plasmin

64
Q

plasmin

A

fragment of plasminogen

65
Q

what are angiogenesis inhibitors designed to prevent?

A

the formation of new blood vessels, thereby stopping or slowing the growth or spread of tumors

66
Q

has the US food and drug administration approved any angiogenesis inhibitors for the treatment of cancer?

A

yes, several

67
Q

side effects of angiogenesis (different than other cancer treatments) (4)

A

bleeding
clots in arteries
hypertension
protein in urine

68
Q

do angiogenesis inhibitors eradicate cancer?

A

no, they only stop or slow the growth of cancer

69
Q

bevacizumab (Avastin)

A

monoclonal antibody that specifically recognizes and binds to VEGF. When VEGF is attached to bevacizumab, it is unable to activate the VEGF receptor. Other angiogenesis inhibitors, including sorafenib and sunitinib, bind to receptors on the surface of endothelial cells or to other proteins in the downstream signaling pathways, blocking the intracellular signaling activities of tyrosine kinase receptors like VEGF receptor.

70
Q

bevacizumab (Avastin) simple mechanism

A

VEGF is unable to bind to its receptor

71
Q

what type of receptors are VEGFR?

A

tyrosine kinase

72
Q

mechanism of action of some anti-cancer angiogenesis inhibitors

A

tyrosine kinase inhibitors which mimic the design of ???? (non competitive inhibitor)

73
Q

dry macular degeneration

A

chronic eye disease that causes vision loss in the center of your field of vision

74
Q

dry macular degeneration is marked by deterioration of the

A

macula

75
Q

macula

A

the center of the retina, the layer of tissue on the inside back wall of your eyeball

76
Q

wet macular degeneration

A

inappropriate angiogenesis occurring in the retina

leakage of blood/fluid into the center of the retina, results in blindness

77
Q

what is the general vascular system of the chorioallantoic membrane of a chick used for?

A

assay materials for angiogenic properties

yolk sac

78
Q

One monoclonal antibody therapy is approved to treat

A

age-related macular degeneration (AMD)

79
Q

age-related macular degeneration (AMD)

A

a progessive eye diease that results in loss of central vision, and is the leading cause of severe vision loss in adults over the age of 65

80
Q

the wet form of AMD accounts for –% of cases

A

10%

81
Q

the wet form of AMD is characterized by

A

the abnormal growth of new blood vessels, which leak fluid and blood, inducing scar formation and destroying vision

82
Q

examples of monoclonal antibody therapy (2)

A

Ranibizumab

Genentech

83
Q

Genentech

A

A recombinant humanized IgG1 kappa monoclonal antibody fragment that binds vascular endothelial growth factor-A (VEGF-A) and cleavage products, and prevents their interaction with VEGF receptors (VEGFR-1 and VEGFR-2), thereby inhibiting endothelial cell proliferation, angiogenesis, and vasular leakage in the retina and choroidal layers.

84
Q

Genentech is approved for (2)

A

neovascular (wet) age-related macular degeneration

macular edema after retinal vein occlusion

85
Q

how is Genentech administered?

A

by intravitreal injection

Applied Biochemistry (52 decks)

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