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Pathology > 3. 7 Growth factors > Flashcards

3. 7 Growth factors Flashcards

1
Q

growth factors

A

are like protooncogenes

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2
Q

cell growth occurs viea

A

auto,
para, and
endocrine actions

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3
Q

auto, para, and endocrine actions work through

A

intrinsic kinase activity (mostly tyrosine kinase),
no kinase activity,
G protein-linked

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4
Q

cell growth requires

A

more than one stimulus/growth factor to grow

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5
Q

No growth factors results in

A

apoptosis

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6
Q

some growth factors results in

A

survival

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7
Q

other growth facotrs results in

A

division

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8
Q

EGF and TGFalpha are

A

epidermal growth factor and transforming growth factor alpha are part of the EGF family and share a common receptor with intrinsic tyrosinge kinase activity

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9
Q

EGF and TGF alpha stimulate

A

a variety of epithelial and mesenchymal cells to proliferate

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10
Q

HGF

A

hepatocyte growth factor/scatter factor

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11
Q

HGF receptor

A

c-met, a frequently mutated protooncogene that has tyrosine kinase activity

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12
Q

HGF is made by

A

mesenchymal cells

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13
Q

HGF stimulates

A

stimulates several types of epithelial cells including hepatocytes and bile duct epithelial cells

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14
Q

HGF promotes

A

embryonic development and scattering/migration of cells

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15
Q

VEGF

A

vascular endothelial growth factor

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16
Q

VEGF family

A

A B C D

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17
Q

VEGF is an inducer of

A

blood vessel formation in embryogenesis wound healing and tumor formation

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18
Q

VEGFR -1, 2, 3

A

3 VEGF receptors with tyrosine kinase activity

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19
Q

VEGFR-2

A

on endothelial cells,
binds VEGF-A,
main role is angiogenesis

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20
Q

VEGF-C and D bind to

A

VEGFR 3 and promote lymphatic development

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21
Q

PGF - Platelet derived growth factor sturcture

A

2 chains of A and B

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22
Q

PGF isoforms

A

AA,
AB,
BB

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23
Q

PGF C and D

A

recently discovered

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24
Q

PDGFR alpha and beta

A

receptors with tyrosine kinase activity

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25
Q

PDGF is made by

A

platelets,
macrophages,
endothelial cells

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26
Q

PDGF induces

A

migration and proliferation of fibroblasts,
smooth muscle cells,
and monocytes

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27
Q

Fibroblast Growht factor is best characterized

A

acidic -: aFGF or FGF1,

basic - bFGF or FGF2

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28
Q

FGF family has

A

10 members

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29
Q

FGF can associate with

A

heparan sulfate in ECM

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30
Q

FGF receptors

A

intrinsic tyrosine kinase activity

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31
Q

FGF is involved in

A

angiogenesis,
wound healing,
myocyte and blood vessel development,
hematopoesis

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32
Q

Transforming Growth factor beta family

A

TGF beta 1, 2, and 3;
BMPs
activins
inhibins

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33
Q

Most widespread TGF

A

TGF beta 1

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34
Q

TGF beta 1 is made by

A

macrophages,
endothelial cells (Ecs?),
lymphocytes and others

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35
Q

TGF receptors

A

type I and type II receptors with serine/threonine kinase activity

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36
Q

TGF receptor binding

A

binds type II first then complexes with type I
then phosphorylates Smad faimily preteins
that transduce signal

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37
Q

Smad

A

potent growth inhibitory signal and loss is associated with unregulated growth and neoplasia

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38
Q

Pleitrophic effects of TGF beta depend on

A

type, concentration, and co factors

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39
Q

TGF beta functions

A

inhibits proliferation of epithelial cells,
upregulates cell cycle inhibitors in some cells,
stimulates proliferation of fibroblasts and smooth muscel cells,
stimulates fibrosis,
anti-inflammatory

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40
Q

receptors with intrinsic kinase activity

A

most growth factor

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41
Q

receptors w/o intrinsic kinase activity that recurit kinases

A

cytokines

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42
Q

7TM gprotein coupled receptors

A

histmaine,
chemotactic,
signals,
epinephrine

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43
Q

Steroid hormone like receptors

A 
in cytosol and nucleus: 
steroids, 
Vit D, 
retinoids, 
PPARs
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44
Q

receptor binding causes

A

receptor anchoring and aggregation

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45
Q

cascade pathways associated with tyrosine kinase

A

Ras-GTP —> MAP kinase,
PI3 kinases —–>AKT kinases,
PLCgammaPIP2 —->IP3 + DAG

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46
Q

PI3 –>AKT kinases are involved in

A

cell survival (inhibition of apoptosis),
proliferation,
insulin signaling

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47
Q

PLC –> IP2 +DAG

A

IP2 –>IP3 causes inc Ca ,

DAG –> activates PKC (Ca also activates PKC)

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48
Q

how does RAS-GTP get activated

A

tyrosine kinase phosphorylation –>GRB2
—>SOS —->RasGDP —->Ras GTP;
adaptor proteins and linker proteins lead to RAS (an oncogene) and binding to ATP makes it active

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49
Q

How does RAS-GTP get shup off

A

intrinsic GTPase activity cleaves terminal phsophate

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50
Q

Down stream signal from Ras-GTP

A

Raf –> MEK –> ERK –> nucleus –>

activation of transcription cFOS, cMYC, cJUN

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51
Q

cFOS, cMYC, cJUN are

A

competence factors and when they are active they allow the cell to get out of G1 and start dividing

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52
Q

Receptors without kinase activity

A

recurit JAK (janus kinase) for downstream signaling via STAT (signal transducers and activators of transcription ) sending signal to the nucleus

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53
Q

G Protein Linked receptors

A

adenyl cyclase - inc cAMP to activate cAMP dependent kinases.
PLC gamma - activates PKC and increases Ca2+

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54
Q

Signal transduction occurs via

A

MAP kinase,
PI3 kinase, IP3 signaling/PKC,
cyclicAMP kinases,
JAK/STAT pathway

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55
Q

Transcription factors have

A

DNA binding zinc fingers

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56
Q

TFs will

A

increase or decrease transcriptin

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57
Q

TF phosphorylation will

A

alter activity

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58
Q

TFs can be

A

protooncogenes/tumor supressor genes (myc, fos, p53)

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59
Q

Growth in serum

A

occurs bc you have coagulation and activated plateltes will secrete a lot of growth factors

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60
Q

Growth in plasma

A

does not occur bc of lack of activate plateltes that secrete growth factors

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61
Q

plasma and PDGF or PDGF and EGF will result in

A

growith bc cells need at least 2 signals, one to get comptence factors activated and another to push the cycle forward

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62
Q

Cyclin dependent kinases are

A

constitutive and are inactive until the appropriate cyclin is produced and then they phosphorylate different proteins

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63
Q

cylin in G1–>S

A

Cyclin E

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64
Q

Cyclin in S–>G2

A

Cyclin A

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65
Q

Cyclin in G2–>M

A

cyclin B

66
Q

CDK + cyclin –>

A

CDK (active)

67
Q

CDK active –>

A

posphorylation of numerous proteins

68
Q

cyclins are degraded by

A

ubiquitine/proteosome complex

69
Q

liver lobes

A

are not perfectly separated so if we cut off one we wont regenerate the full part we cut off

70
Q

Kupfer cells and endothelial cells of sinusoids in liver make

A

TNF and IL6

71
Q

insuline and norepinephrine are

A

adjuvants in the cell cycle making it more robust to get to S phase

72
Q

G0 –> G1

A

Liver NPCs,
TNF,
IL6,
cFOS, cJUN, cMYC–>AP1–>NFkB,Stat3

73
Q

G1–>S

A 
HGF, 
TGFalpha, 
Insulin, 
NE, 
Bcl-X
74
Q

S –> M

A

cyclins,
CDK4,
CDK2

75
Q

TGFbeta and activin

A

inhibition of cell cycle/ epithelial growth

76
Q

Extracellular matirx is made of

A

collagens (1-9),
elastin/fibrilin,
glycoproteins ,
proteoglycans

77
Q

glycoproteins in ECM

A

fibronectin,
laminin,
integrins

78
Q

Proteoglycans in ECM

A

heparan and chondroitin sulfate,

hyaluronic acid

79
Q

ECM is a

A

skeleton,
intracellular glue,
potent signaling pathway

80
Q

ECM has

A

interstitial matirx,
basement membrane, and
provisional matrix

81
Q

ECM interstitial matrix

A

fibrillar and nonfibrillar collagen,
elastin, and
varying amounts of other constituents

82
Q

ECM Basement membranes

A

epithelial cell contact,
amorphous nonfibrillar collagen (4),
laminin, and
others

83
Q

ECM provisional matrix

A

temporary accumulation of ECM at sites of injury

84
Q

what is the most abundant animal protein

A

collagen

85
Q

collagen structure

A

triple helix of 3 alpha chains

86
Q

collagen synthesis

A

chains undergo hydroxylation reactions that need VitC.

87
Q

Collagen modification post secretion

A

cleavage and crosslinking

88
Q

types of collagen

A

27 types encoded by 41 genes over 14 chromosomes - huge genetic target

89
Q

no Vit C

A

you don’t heal bc no collagen syn

90
Q

full steps of collagen syn

A 
alpha chain syn off ribosome, 
hydroxylation, 
glycosilation, 
alphachain arrangement inot tripple helix, 
clipping of N and C term peptides, 
crosslinking
91
Q

why the crosslinking?

A

makes it stiffer

92
Q

type 1 collagen

A

high tensile strength

93
Q

type 1 collagen is found in

A

skin, bone, tendons, most organs

94
Q

type 2 collagen

A

thin fibrils, sturctural protein

95
Q

type 2 collagen is found in

A

cartilage, vitreous humor

96
Q

type 3 collagen

A

thin pliable

97
Q

type 3 collagen is found in

A

blood vessels, uterus, skin

98
Q

type 4-6 collagen

A

amorphous

99
Q

type 4-6 collagen is found in

A

basement membrane and interstitial tissues

100
Q

type 7

A

anchoring filament

101
Q

type 7 found in

A

dermal-epidermal junction

102
Q

type 8

A

endothelium-descement membrane

103
Q

type 9

A

cartilage

104
Q

Elastin is found in

A

vessels, skin, uterus, lung

105
Q

Elastin can

A

stretch then snap back

106
Q

Elastin sturcture

A

central core protein (elastin) surounded by fibrilin

107
Q

Elastin elasticity controlled by

A

crosslinking

108
Q

Most insoluble and resistant to break down protein

A

elastin

109
Q

In arterial walls elastin is

A

slowly replaced

110
Q

Adhesive glycoproteins

A

bind ECM and to cell receptors - like glue

111
Q

adhesive glycoprotein examples

A

fibronectin and laminin

112
Q

fibronectin is found in

A

many locations and serum -helps cells bind and grow better

113
Q

laminin is found in

A

basement membranes

114
Q

Fibronectin size

A

very large 450 kDa secreted by many cell types like the liver

115
Q

fibronectin binds

A

many cells especially endothelial cells, via a receptor that recognizes the tripeptide sequence
RGD (argenin,glycine,aspartat)

116
Q

fibronectin directly mediates

A

attachment spreading and migration of cells and modifies responses to growth factors

117
Q

RGD motif on fibrin binds

A

integrins on endothelial cells

118
Q

fibrin has binding domains for

A

heparan,
fibrin,
collagen and
integrins

119
Q

laminin size

A

very large 820kDa

120
Q

what is the most abundant glycoprotein in the basement membrane

A

laminin

121
Q

laminin spanns the basement membrane and binds

A

integrins on cells

122
Q

laminin binds

A

collagen 4 and heparan sulphate in basement membrane

123
Q

laminin mediates

A

spreading,
adhesion,
alignment, and
responses to growthfactors

124
Q

if you destroy laminin

A

you lay down type 1 collagen instead of type 4 and you scar. You’ll fill the hole but won’t resolve.

125
Q

cell adhesion proteins/molecules

A

immunoglobulin family,
cadherins,
integrins,
selectins

126
Q

Ig family CAMs

A

same or different cell type interactions

127
Q

Caderhin CAMs

A

Ca dependent same cell interactions (like btw columnar cells for ex)

128
Q

Integrin CAMs

A

very broad range of binding cell-cell and cell-ECM

129
Q

Selectin CAMs

A

C-type lectin involved in leukocyte endothelial binding

130
Q

Cadherins occur at

A

zona adherins and desmosomes

131
Q

Cadherin linkage with

A

cytoskeleton through alpha and beta catenin

132
Q

cadherins modulate

A

proliferation,
differentiation, and
motility (contact inhibition of replication)

133
Q

beta catenin is an important inducer of

A

colon carcinoma

134
Q

if cadherins are taken away

A

loss of contact inhibition resulting in neoplasia

135
Q

Integrins

A

cell receptors that bind to adhesive proteins (ex RGD seq of fibronectin)

136
Q

Integrins are linked to

A

cytoskeleton and signal transduction pathways

137
Q

alpha integrins

A

14 subtypes

138
Q

beta integrin chain

A

8 subtypes

139
Q

integrin chain chain

A

alpha and beta

140
Q

integrins are found on

A

many cells

141
Q

integrins mediate

A

leukocyte adhesion,
platelet aggregation,
wound healing

142
Q

some cells undergo apoptosis if

A

thye are not bound to the matrix by integrins

143
Q

Matricellular protein examples

A

SPARC,
Thrombospondins,
Osteopontin,
Tenacin

144
Q

Matricellular Proteins

A

nonstructural components of ECM but modify cell-ECM interactions

145
Q

Matricellular Protein - SPARC

A

secreted protein acidic and rich in cystien aka osteonectin

146
Q

SPARC is involved in

A

tissue remodling,
inhibits angiogenesis,
(Ca++?)

147
Q

Thrombospondins

A

inhibit angiogenesis

148
Q

Osteopontin

A

Ca2+,

leukocyte migration

149
Q

Tenacin

A

cell morphogenesis and

cell adhesion

150
Q

Proteoglycans

A

protein linked to polysaccharides containing a sulfate -

along with hyaluronana are the 3rd general sturctural component of ECM

151
Q

Proteoglycan examples

A

heparn sulfate,
chondroitin sulfate,
dermatan sulfate

152
Q

proteoglycans are named by

A

the repeating disaccharide

153
Q

proteoglycans can also be

A

cell membrane proteins like Syndecan

154
Q

Syndecan

A

spans membrane and binds GFs and ECM and interacts with actin

155
Q

Hyaluronan is made of

A

simple end to end disaccharide repeats

156
Q

hyaluronan binds to

A

many receptors including CD44 that mediates migration and proliferation

157
Q

unique feature of hyaluronan is that it binds

A

massive amouns of H2O thus excellent cushion effect so found in joints

158
Q

hyaluronan inhibits

A

cell-cell adhesion and facilitates cell migration

159
Q

heparan sulfate binds

A

FGF that finds the FGF receptor

160
Q

the same growth factors and cells in varied ECM will

A

vary the response

Pathology (26 decks)

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