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54 Cards in this Set

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Can sensory & motor nerves regenerate? What are their limits?
Yes, if the endoneurial tubes encasing the nerves remain intact and inregister at the site of injury. The ends of the axons on the proximal side of the injury are sealed off and their distal part degererates. The sealed proximal segment of the axon then sprouts an advancing growth cone, behind which the axon extends through the endoneurial tube to make new synapses with target skin and muscle.
Mitotically competent cells?
Cells that have the receptors and signal transduction pathways to respond to a regeneration-permissive environment
What are the 3 pre-req’s needed for regeneration at the tissue level?
1. Mitotically Competent Cells
2. Regeneration Promoting Signals Present: Injury environment must contain signals necessary to promote the proliferation and differentiation of the regenerative cells
3. Regeneration Inhibiting Signals Absent: suppressed or neutralized
What are the three mechanisms of regeneration at the tissue level?
Compensatory hyperplasia of differentiated cells

Activation of resident ASCs that self-renew within a specific micro niche

Creation of regeneration competent cells by dedifferentiation (amphibians & fish)
Compensatory Hyperplasia
Proliferation occurs while maintaining differentiated functions

Liver (Hepatocytes)
Pancreas


Example: liver
Natural Regeneration via ASCs
i. Resident undifferentatiated cells
ii. Self renewing, many divide asymmetrically
iii. 2 main types:
Epithelial stem cells
Mesodermal Stem Cells
Erythrocytes need what for apoptosis?

*from book
absence of erythropoietin
what are "pro-life" signals & what do they do?
GF, Cytokines, other Niche Factors

--> expression of BCL-2 on the outside of the Mito that protects/ stabilizes it
this gene family is part of the "pro-life" gene family
Bcl-2 family: Bcl-2 & Bcl-x
Direct death signals (Reapers) are caused by?
DNA damage
TNF-alpha
Hypoxia
Cell stress
Exercise to exhaustion
Death signals cause increase?
BAD, BAX
what do BAD, BAX do?
Destroys Bcl-2 --> destabilizes Mito membrane
destabilization of Mito membrane leads to what?
leakage of cytochrome c
leakage of cytochrome c leads to what?
activation of APAF-1 (Apoptotic Protease Activating Factor 1)
What does APAF-1 do?
activates Caspase-9
What does capsase 9 do?
activates caspase 3,7

--> digest cell
walk through the cell death pathway
Death Signals (TNF-alpha) increase Bad, Bax
1. BAD, BAX destroy Bcl-2 on Mito membrane
2. cytochrome c leaks & activates APAF-1
3. APAF-1 activates caspase-9
4. caspase-9 activates caspase-3,7 & digests cell
life & death genes were first discoved in ?
C. elegans
What are the strategies of regenerative medicine?
1. Cell Transplantation

2. Bioartificial Tissues

3. Induction of Regeneration In Situ
Morphallaxis
Hydra
regeneration of missing parts w/out growth -->
repatterning the remaining tissue into a proportioned but small whole, then growth
Epimorphosis
proliferation of stem or progenitor cells, followed by ther differntiation into the tissues that were lost

differentiation linked to growth
Epimorphosis occurs in
flatworms, annelid worms

amphibian appendages/jaw

deer antlers, rabbit ear tissue, fetal digits
Pick up on stratagies of regen
3 Sep 2009
3 sep 2009
Fibroblasts synthesize 3 proteins in ECM
Proteoglycan

Fiberous Proteins

Adhesive Proteins
Proteoglycan
part of ECM-Dermis

GAGs, bind HA & together trap water-> skin resists compression
Fiberous Proteins: synthesized by Fibroblasts in the dermis
a. Types 1 & 3 collagens, gives skin tensile strength
b. Collagen VI (six): stabilizes blood vesseles
c. Elastins: is stretchy, gives skin elasticity
Adhesive proteins
these provide a substrate for cell migration
a. Fibronectin
b. Tenascin
c. Vitronectin: associated w/elastins
Skin Basement membrane is btw
Stratum Basal of Epidermis & Papillary layer of Dermis
3 basic phases of repair
1. Hemostasis
2. Inflammaiton
3. Structural Repair
Tissue Factor Pathway
caused by 2nd Hemostasis
TF is a membrane spanning protein that initates cascad
1. TF:F7 --> activates F10
2. F10 cleaves F5 --> Prothrombin --> Thrombin
Inflammation: What degrades the damaged collagen?
MMP1,8
matrix metallo proteases
Tissue Plasminogen Activator
Angiogenesis:used by endothelial cell to get into wound

Converts Plasminogen ->Plasmin
Plasmin dissolves Fibrin
What do fibroblasts do to get to wound
secrete MMPs
This will induce macrophage apoptosis
VEGF
Vascular Endothelial Growth Factor
causes the epidermis to thicken vertically by mitosis
FGF7

produced by Fibroblasts
what do fibroblasts do during Formation of granular tissue?
Open up: MMP & HA

Fibronectin & Collagen1

FGF7 causing epidermis to proliferate
lysyl oxidase
causes Collagen1 to crosslink parallel with wound
Remodel granular tissue into scar: this causes 'dieback'
decreased EGF --> acellular fiberous pathc (scar
Hemostasis: what do platelet secrete that causes Inflammation & re-epithelization ?
TGF-beta
PDGF1,2,3
during inflammation pithlia secrete this which causes proliferation
EGF
RTK ligands
Used by the GF FGF, PDGF, EGF, VEGF, and SCF.
macrophages secrete these during inflammation taht act on the Epi
EGF, TGF-alpha, IL-1
neutrophils secrete these during inflammation that act on Epi
EGF, TGF-alpha, HGF
Macrophages secrete these that affect fibroblasts during inflammation
TGF-beta1,2: Migration

TGF-beta3 Proliferation
Fetal skin, Unlike adult has these things that promote regen over fibrosis
Low TGF-beta 1,2
High TGF-beta 3
trasiently IL-6
nude mice that can regenerate have these signals
High HA
Low: TGF-beta1,2; Collagen1
macrophages & plateltes secrete these mitogenic factors for schwann cells
FGF
PDGF
TGF-beta
IL-1,2,6
Inf-gamma
chwann cells secrete these for neuron survival & elongation
NGF
VDNF
NT3,4
CNTF
GDNF
growth cone follows these adhesive factors from schwann cells
N-CAM
N-CAD
L1
Ln, Fn
NoGO pathway
causes growth cone to collapse
ligand binds NoGo receptor
1. activates RhoA (exchagnes GDP for GTP)
Which leads to depolimerization of growth cone
these activate NoGO receptor
MAG
Olgiodendrocyte myelin
CSPGS
Ephrin B3
Tanacin R
NoGo
4 major TF are always present in hepatocytes
a) Liver specific form of NF2B (PHF)
b) STAT3: Signal Transducer & Activator of Transcription 3
c) AP-1
d) C/EBPβ
• Delayed Early Genes
activated during Progession phase of liver regen
1. CDK P-lates Rb
2. E2F disassociates from Rb
--> E2F drives cell into G1
Liver regen needs 3 GF pathways
1. HGF Pathway
2. EGF/TGF-alpha
3. TGF-alpha/IL6