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71 Cards in this Set

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  • Back
angiogenesis
blood vessel formation in adults (critical to chronic inflammation, tumor growth and to vascularization of ischemic tissues)
precursor of collagen? comes from?
PROCOLLAGEN (secreted by cells and cleaved into collagen)
Firbillar Collagens
Types I, II, III, and V
In terms of wound healing, probably the most important type of collagen
Type IV Collagen, (BM type)
ubiquitous collagen type, most abundant, found in skin, bone, and many other tissues (hard and soft)
Type I collagen
Type II collagen
CARTILAGE
Type III cartilage is a component of...
hollow organs and soft tissues
Type V collagen is found in what types of tissues?
soft tissues
and
blood vessels
BM components
Type IV collagen
Laminin
Entactin
Haparin Sulfate Proteoglycan
type of collagen found in intervertebral disk cartilage
Type IX volalgen
firbonectin
large protein, binds to many molecules (eg: integrins, heparin, collagen, fibrin, proteoglycans and cell-surface receptors)
2 types: TISSUE FIBRONECTIN and PLASMA FIBRONECTIN
protein that forms fibrillar aggregates at wound healing sites
Tissue fibronectin
protein that forms initial wound filling clot (serves as substrate for ECM deposition)
Plasma form of Fibronectin
most abundant glycoprotein in the BM
Laminin
Laminin
most abundant glycoprotein in the BM

has binding domains for both ECM and cell-surface receptors (binding sites for Type IV collagen, cell, heparin sulfate proteoglycan)
granulation tissue
the perfused, fibrous connective tissue that replaces a fibrin clot in healing wounds
(VEGF promotes angiogenesis and + vascular permeability, exudation and deposition of plasma proteins (eg fibrinogen and plasma fibronectin in the ECM) provides a stroma for fibroblast and endothelial cell growth
these trigger migration to site of injury and subsequent proliferation of fibroplasts
GROWTH FACTORS
examples of GROWTH FACTORS involved in wound healing:
TGF-beta, PDGF, EGF, FGF and cytokines IL-1 and TNF.

sources: platelets, MOs and activated endothelial cells
regeneration
requires: INTACT TISSUE SCAFFOLDING (esp. BM) new cells in tissue/organ derived from division of stabile cells or new cells from stem cells **restores tissue to NORMAL STATE
healing
occurs when tissue scaffolding has been altered or destroyed, involves combination of creation of new tissue cells and collagen deposition (fibrosis/scarring) **normal state never totally re-established
scar
composed of spindle shaped fibroblasts, dense collagen, fragements of elastic tissue and other ECM components
what happens as a scar matures?
vascular regression continues, eventually transforming the richly vascular granulation tissue to a pale avascular scar
what are the 3 normal cell types (in terms of their turnover)
LABILE: continually replaces
STABILE: not dividing, but can divide
PERMANANT: cannot divide
cell proliferation is regulated by what 3 factors?
a) hormonal influences
b) growth stimuli (during growth years)
c) pathological stimuli
cell devision in most stabile cell populations is governed by what 3 factors?
a) soluble stimulatory factors
b) soluble INHIBITORY factors
c) cell-cell contact (eg: contact inhibition)
increasing cell proliferation to repair damage can occur by what 3 mechanisms?
a) shortening the cell cycle (proliferate faster)
b) pushing stabile cells into the cell cycle
c) stimulating stem cells to generate parenchymal cells
TRANSMEMBRANE SIGNALING is a critical feature in tissue repair. What kind of membrane receptors are involved?
-RTKs (receptors with kinase activity, typically bind: GFs)
-Receptors w/o kinase activity (typically bind CYTOKINES and INTERLEUKINS)
-GPCRs (7 transmembrane proteins, bind CHEMOKINES)
ECM components
COLLAGENS (I, II and IV)
PROTEINS (that connect cells to ECM, laminin, fibronectin, integrins)
GAGs (glycosaminoglycans: heparan suflate, dermitan sulfate, etc..)
a FIBROPROLIFERATIVE RESPONSE that PATCHES rather than restores tissue
HEALING
Basic Steps in TISSUE REPAIR
1) CLOTTING (fibrin deposition) if needed; 2) INFLAMMATION and DECONTAMINATION (M0s); 3) RELEASE of CHEMOATTRACTANTS AND GFs; 4) MIGRATION/PROLIFERATION of FIBROBLASTS; 5)PRODUCTION of ECM materals 6)ANGIOGENESIS; 7)REMODELING of ECM/COLLAGEN; 8)CONTRACTION 9) APOPTOSIS of FIBROBLASTS in MATURE SCAR
Pathways (involved in would healing) associated with Receptors with Tyrosine Kinase Activity
PI3 Pathway
MAP-Kinase Pathway
IP3 Pathway
(all affect Transcription Factor activity)
cAMP pathway is activated by what type of receptor?
GPCRs (typically bind CHEMOKINES: eg serotonin, histamine)
JAK/STAT pathway is activated by what?
CYTOKINES
chemokines signal ax membranes via what type of receptors?

what kind of intracellular change results?
GPCRs

causing release of Ca2+
and/or
generation of cAMP
stabile cells are in what phase of cell cycle?
Go
Where are the two major cell cycle checkpoints for DNA damage?
G2/M checkpoint: for damaged or unduplicated DNA
G1/S checkpoint: for DNA damage
What is CDK1? What does it do?
Cyclin depedent kinase 1 (produced constituitively, but requires cyclinB for activity)
when bound to cyclin B, works as TRANSCRIPTION FACTOR (pushes cell from S phase to G2)

phosphorylation, associated with G2/M checkpoint
during what phase is the RESTRICTION POINT of the cell cycle?
G1 (Pre-synthetic phase)
Over what timeframe do the following events occur following tissue injury?
INFLAMMATION
GRANULATION TISSUE formation
WOUND CONTRACTION
INFLAMMATION (0-3 days)
GRANULATION TISSUE formation (0.3-10 days)
WOUND CONTRACTION (3-50 days)
What is HEALING BY 1st INTENT?
wound edges apposed (better result than if apart)
Healing by "2nd INTENT"
wound edges apart, or loss of tissue (increased scar)
TRANSMEMBRANE SIGNALING is a critical feature in tissue repair. What kind of membrane receptors are involved?
-RTKs (receptors with kinase activity, typically bind: GFs)
-Receptors w/o kinase activity (typically bind CYTOKINES and INTERLEUKINS)
-GPCRs (7 transmembrane proteins, bind CHEMOKINES)
ECM components
COLLAGENS (I, II and IV)
PROTEINS (that connect cells to ECM, laminin, fibronectin, integrins)
GAGs (glycosaminoglycans: heparan suflate, dermitan sulfate, etc..)
a FIBROPROLIFERATIVE RESPONSE that PATCHES rather than restores tissue
HEALING
Basic Steps in TISSUE REPAIR
1) CLOTTING (fibrin deposition) if needed; 2) INFLAMMATION and DECONTAMINATION (M0s); 3) RELEASE of CHEMOATTRACTANTS AND GFs; 4) MIGRATION/PROLIFERATION of FIBROBLASTS; 5)PRODUCTION of ECM materals 6)ANGIOGENESIS; 7)REMODELING of ECM/COLLAGEN; 8)CONTRACTION 9) APOPTOSIS of FIBROBLASTS in MATURE SCAR
Pathways (involved in would healing) associated with Receptors with Tyrosine Kinase Activity
PI3 Pathway
MAP-Kinase Pathway
IP3 Pathway
(all affect Transcription Factor activity)
cAMP pathway is activated by what type of receptor?
GPCRs (typically bind CHEMOKINES: eg serotonin, histamine)
JAK/STAT pathway is activated by what?
CYTOKINES
chemokines signal ax membranes via what type of receptors?

what kind of intracellular change results?
GPCRs

causing release of Ca2+
and/or
generation of cAMP
stabile cells are in what phase of cell cycle?
Go
Where are the two major cell cycle checkpoints for DNA damage?
G2/M checkpoint: for damaged or unduplicated DNA
G1/S checkpoint: for DNA damage
What is CDK1? What does it do?
Cyclin depedent kinase 1 (produced constituitively, but requires cyclinB for activity)
when bound to cyclin B, works as TRANSCRIPTION FACTOR (pushes cell from S phase to G2)

phosphorylation, associated with G2/M checkpoint
during what phase is the RESTRICTION POINT of the cell cycle?
G1 (Pre-synthetic phase)
Over what timeframe do the following events occur following tissue injury?
INFLAMMATION
GRANULATION TISSUE formation
WOUND CONTRACTION
INFLAMMATION (0-3 days)
GRANULATION TISSUE formation (0.3-10 days)
WOUND CONTRACTION (3-50 days)
What is HEALING BY 1st INTENT?
wound edges apposed (better result than if apart)
Healing by "2nd INTENT"
wound edges apart, or loss of tissue (increased scar)
complications of wound healing process
1) SCAR ITSELF (esp. parencymal scarring of organ)
2) KELOIDS
3) CONTRACTURES (collagen maturation/contraction)
4) ULCERATION (incomplete healing)
factors determining outcome/effectiveness of healing
-extent of damage
-if healing by 1st or 2nd intent
definition of wound
disruption of tissue continuity
scap
coagulated mtaerial that has accumulated in a wound
ESCHAR
scab-like lesion on the skin following a burn
GRANuLATION TISSUE
early scar tissue
KELOID
exaggherated type of scar formation
CICATRAX
scar
coagulation factors active in would repair
HAGEMAN FACTOR FRAGMENTS (vasopermeability)
BRADYKININ (vasodilation, permeability, pain)
COMPLEMENT (leuocyte recruitment, vasopermeability)
FIBRIN CLOT (hemostatic plug, reservoir of GFs, provisional matrix for cell migration)
role of platelets in wound repair
ADHESION (plug small leaks in vessls)
AGGREGATION (plug large leaks, induce coagulation)
MEDIATOR RELEASE (vasoconstriction, stimulates additional aggregation of platelets and GF release)
GFs active in wound healing
FGF1 & 2
PDGF
TGF-beta
VGEF
FGF1&2
Fibroblast Growth Factors
active in wound healing (fibroblast and epidermal cell proliferation and angiogenesis)
PDGF
platelet derived growth factor
active in wound healing
involved in fibroblast chemotaxis, proliferation and contraction
TGF-beta
TRANSFORMING GF beta
involved in wound healing
fibroblast chemotaxis
ECM deposition
protease inhibitor secretion
VGEF
Vascular Endothelial Growth Factor
involved in vascular permeability, angiogenesis