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MCM Final Exam > MCM Final - Angiogenesis > Flashcards

MCM Final - Angiogenesis Flashcards

0
Q

endothelial cells

A

single layer of cells that lines vessels

localizes immune system and response to ischemic environment
-important roles

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1
Q

where are vessels derived from? (cell type)

A

mesoderm

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2
Q

cells in vessels

A

endothelial cells, basal lamina, connective tissue and smooth muscle, and pericytes

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3
Q

basal membrane in blood vessels

A

ECM laid down for support and to create barrier

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4
Q

smooth muscle in vessel?

A

only larger ones, not capillaries

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5
Q

pericyte

A

extends processes that surround the capillary

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6
Q

vasculogenesis

A

during embryonic development

-primitive vascular network from endothelial and hemopoetic precursors

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7
Q

angiogenesis

A

vessel formation during adulthood

-growth by new vessels sprouting from existing ones

during pathology**

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8
Q

angioblast

A

endothelial cell precursor

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9
Q

VEG-F

A

released by mesenchymal cells causing vasculogenesis

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10
Q

neovascularization

A

aka angiogenesis

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11
Q

capillary sprout

A

originates from existing capillary cell

tip cell - at tip of sprout (not dividing)

stalk cell - follow tip cell, form hollow lumen (actively dividing)

continues growing until reaches another sprout or vessel

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12
Q

tip cell

A

does not divide

has filopodia

begins formation of capillary sprout (from existent endothelium cell)

responds to guidance signals (semaphorins, slits, netrins, ephrins)

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13
Q

stalk cells

A

follows the tip cell during angiogenesis

actively dividing
-forms a hollow lumen

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14
Q

EPCs

A

endothelial precursor cells

migrate from bone marrow
-express VEGFR-2 and VE-cadherin

not necessary for angiogenesis

in ischemic patients - increase in number of EPCs

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15
Q

Process of Angiogenesis

A

1 vasodilation
-nitric oxide (NO) and VEGF dilate the area
2 degradation
-proteolysis of basement membrane (MMPs)
3 migration
-of endothelial cells in direction of growth
-growth factors or inhibitors
4 proliferation
-of endothelial cells
5 maturation
-when make contact with another stalk cell or vessel
-laying down basement membrane, recruiting pericytes, and maybe smooth muscle cells

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16
Q

MMPs

A

matrix metalloproteinases

-cause the degradation of the vessel basement membrane during angiogenesis

plasminogen activator

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17
Q

VEGF-A

A

vascular endothelial growth factor

acts as paracrine ligand

diffuse and interacts with VEGFR-2 receptor

- downstream signaling pathway
- tyrosine kinase receptor
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18
Q

VEGFR-2

A

ligand is VEGF-A

tyrosine kinase receptor

leads to EPC migration from bone marrow, increased vascular permeability, endothelial cell survival and proliferation/motility, upregulate express of pro-angiogenic proteins

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19
Q

pro-angiogenic proteins upregulated by VEGF-A?

A

plasminogen activator
collagenase

don’t worry about these too much - will learn later

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20
Q

what induces VEG-F?

A

hypoxic conditions

- tissue needs more oxygen
- done through Hif1 - expressed due to lack of oxygen
21
Q

Notch receptor in angiogenesis

A

juxtacrine signaling

receptor expressed in stalk cells

allows us to control excessive proliferation of endothelial

decreases cells responsiveness to VEGF

ligand is delta - expressed by the tip cells

22
Q

delta (ligand)

A

secreted from tip cells in response to VEGF activation

bind the notch receptor on the stalk cells

- results in decreased responsive to VEGF
- decrease in branching and proliferation of endothelial stalk cells
23
Q

angiopoietins

A

Ang1 and Ang2 function in opposite ways

24
Q

Ang1

A

latter steps during maturation of vessel during angiogenesis

recruits pericytes and smooth muscles

25
Q

Ang2

A

antagonist of Ang1

binds same receptor and acts as an inhibitor
-continues to allow the endothelial cells and limits the maturation of the vessels during angiogenesis

26
Q

PDGF

A

platelet-derived growth factor

secreted by the endothelial cells and platelet cells

PDGFR is the receptor (on pericytes and smooth muscle)

release after Ang1 signaling

27
Q

bFGF

A

basic fibroblast growth factor

from endothelial cells and macrophages

secreted and stored in the ECM
-has affinity for heparin

causes induction of mitosis

28
Q

bFGFR

A

receptor for bFGF

- expressed on endothelial cells, fibroblasts, smooth muscle cells, neurons
- induces mitosis
29
Q

TGF-beta

A

transforming growth factor

induces VEGF expression
-on fibroblasts and endothelium

30
Q

MMPs

A

matrix metalloproteinases

contains zinc

diverse family of enzyme

any type of tissue remodeling

secreted as zymogens (inactive) - because they are dangerous

release induced by VEGF, inflammation or damage

31
Q

integrin signaling during angiogenesis

A

transmembrane receptor integrin binds juxtacrine ligandes

- group together and form focal adhesion complexes
- leads to intracellular signaling cascase
32
Q

focal adhesion complexes

A

integrin bound to juxtacrine ligand during angiogenesis

33
Q

thrombospondin-1

A

inhibitor of angiogenesis

upregulated by p53

functions in ending the process of angiogenesis

34
Q

mutation in what protein can promote angiogenesis?

A

p53

35
Q

Hif-1 alpha

A

induces the expression of VEGF

36
Q

angiostatin

A

inhibitor of angiogenesis

internal fragment of plasminogen (in circulation)

- plasminogen degrades bc of MMPs
- releasesfragment of angiostatin

inhibits endothelial cell migration and division

37
Q

endostatin

A

inhibits angiogenesis

fragment of collagen released due to MMP activity
-inhibits VEGF signaling

38
Q

platelets

A

fragmented portions of cells

protein sack that is released

14 promoters and 12 inhibitors

when reaches injured area or clot

- regulators released in sequence
	- pro-angiogenic and later anti-angiogenic sequence
	- help with the maturation process in tissue
39
Q

down regulation of angiogenesis?

A

high levels of oxygen leads to degradation of Hif1

no VEGF - no angiogenesis

VHL (von hippel lindau) marks Hif1 for degradation

40
Q

VHL

A

von hippel lindau

E3 ubiquitin ligase that marks Hif1 for degradation

41
Q

Von Hippel Lindau Sydrome

A

mutation in VHL leads to nonfunctioning protein

- cannot degrade Hif1
	- therefore, constitutively expression of VEGF

leads to hemangioblastoma - blood vessel dense tumor

42
Q

hemangioblastoma

A

blood vessel dense tumor

result of von hippel lindau syndrome

43
Q

non-neovascularized tumor

A

not clinically detectable (except surface lesion)

small size

slow growth

benign

44
Q

neovascularized tumor

A

tumor has ability to control capillary growth

can secrete angiogenic proteins
-induce capillary sprout growth

45
Q

two way paracrine exchange in tumors

A

tumor - angiogenic proteins
-vessel growth to tumor
endothelial - chemoattractants
-tumor migration to blood vessel

46
Q

direct drugs inhibiting angiogenesis?

A

acting on the endothelial cells to inhibit their response

ex./ bevacizumab (avastin)

47
Q

indirect drugs for angiogenesis?

A

inhibits tumor from secreting pro-angiogenic proteins

ex./ trastuzumab (herceptin)

48
Q

Bevacizumab

A

aka avastin
direct drug for inhibiting tumor angiogenesis

anti-VEGF antibody

used in diabetic retinopathy treatment

49
Q

diabetic retinopathy treatment?

A

use bevacizumab

-intravitreal injection that causes the inhibition in vascularization of the eye

50
Q

Trastuzumab

A

(aka herceptin)
-indirect

breast cancer treatment

- Her-2/neu are tyrosine kinases that are overexpressed or mutated in breast cancer
	- ligand - not known
	- activation results in pro-angiogenic factor secretion

drug acts as antibody antagonist

MCM Final Exam (16 decks)

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