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FM 1 > Regeneration, Repair, and Wound Healing > Flashcards

Regeneration, Repair, and Wound Healing Flashcards

1
Q

regeneration

A
  • restoration of damaged or lost cells or tissues to their original state
  • requires cell proliferation (parenchyma or stem cell pop) and an intact ECM scaffold
  • eg normal/homeostatic replacement of skin cells
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2
Q

repair

A
  • involves a combination of regeneration and scar formation by collagen deposition
  • requires cell proliferation; ECM is usually damaged and new ECM (collagen) is deposited
  • eg burn healing
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3
Q

regulation of cell cycle

A
  • G1-S checkpoint
  • cylicns (D) bind to cyclin dependent kinase ->form heterodimer -> phophorylate retinoblastoma protein -> release E2F -> protein transcripton
  • CDK inhibited by growth inhibitors (TGF-B, p53), activated by growth factors (EGF, PDGF)
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4
Q

growth factors

A
  • polypeptides that bind cellular receptors and stimulate cell proliferation
  • can also stimulate cytoskeletal rearrangement (alter cellular motility and contractility), cellular differentiation, angiogenesis
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5
Q

Epidermal growth factor (EGF)

A
  • includes EGF, TGF-a
  • receptor EGRF1, tyrosine kinase, juxtacrine
  • from macrophages, inflammatory cells, platelets
  • acts on epithelial cells, fibroblasts
  • effects cellular proliferation
  • diseases: psoriasis (TGF-a), Her2 receptor + breast cancer
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6
Q

Platelet derived growth factor (PDGF)

A
  • secreted proteins
  • PDGRF a and B, receptor tyrosine kinase
  • from platelets, macrophages, endothelial cells, fibroblasts
  • acts on mesenchymal cells (hematopoietic cells, fibroblasts)
  • primary chemokine and mitogen for mesenchymal cells, stimulates fibroblasts to secrete ECM and collagenase, attract inflammatory cells-secrete growth factors
  • chronic eosinophilic leukemia-receptor gene fusion-uncontrolled eosinophil proliferation
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7
Q

Fibroblast growth factor (FGF)

A
  • receptor tyrosine kinase; FGF must be bound to extracellular matrix to activate
  • from macrophages, endothelial cells
  • target fibroblasts, endothelial cells
  • fibroblast chemotaxis and proliferation, ECM deposition, angiogenesis
  • lots of diseases
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8
Q

Vascular endothelial growth factor (VEG-F)

A
  • polypeptide growth factors
  • receptor tyrosine kinase
  • from variety of mesenchymal cells (leukocytes and fibroblasts)
  • target endothelial cells
  • angiogenesis, endothelial cell proliferations and migration, increase vascular permeability
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9
Q

Transforming growth factor B (TGF-B)

A
  • polypeptide growth factors
  • receptor serine/threonine kinase
  • from platelets, endothelial cells, fibroblasts, macrophages, lymphocytes
  • target fibroblasts, leukocytes
  • multiple opposing effects: promotes fibrogenesis, stimulate fibroblast and smooth muscle proliferation, inhibit epithelial and mesenchymal cell growth, strong anti-inflammatory agent, attract neutrophils, fibroblasts, macrophages
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10
Q

Interferon

A
  • cytokine
  • from T-cells
  • target macrophages and fibroblasts
  • role in wound healing: activates macrophages (major mediator of wound healing), down regulates collagen synthesis, inhibit fibroblast proliferation
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11
Q

Interleukin-1

A
  • cytokine
  • from macrophages
  • target inflammatory cells and fibroblasts
  • wound healing: mediates inflammatory cell fxns in wound, neutrophil and fibroblast chemotaxis
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12
Q

Tumor necrosis factor

A
  • cytokine
  • from macrophages and t-cells
  • target macrophages and t-cells (autocrine)
  • wound healing: activates macrophages, stimulate IL-1 production, activate t-cells, induce collagen production in fibroblasts, attract neutrophils
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13
Q

Embryonic stem cells

A
  • derived from inner cell mass of blastocyst
  • each cell is pluripotent
  • have self renewal capacity
  • uses-treatment of ds where there is a loss of critical cell types (MI, Alzheimers, Parkinsons, spinal cord injury, DM type 1)
  • challenges- ethical issues, transplant rejection, tumor formation (teratoma), persistence of underlying ds, making differentiated cells fxn normally
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14
Q

induced pluripotent stem cells

A

-skin cells -> transduce in certain genes -> proteins -> induce cells back to pluripotent state

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15
Q

Adult stem cells

A
  • small reservoirs of self-renewing cells in multiple tissues
  • restricted in their differentiation potential
  • fxn is to regenerate cells lost by normal wear and tear (hair follicle, GI crypts, liver, eye)
  • if moved to different tissue, can transdifferentiate in vitro; otherwise restricted niches
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16
Q

ECM fxns

A
  • provide turgor by sequestering water or rigidity by sequestering minerals
  • reservoir for secreted growth factors
  • framework for cells to adhere, migrate and proliferate in
  • mediates cell-cell interactions
  • site of remodeling during wound healing
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17
Q

ECM composition

A
  • fibrous structural proteins
  • adhesive glycoproteins
  • proteoglycans and hyaluronic acid
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18
Q

Col I

A

most common type in mammals
bone, tendon, mature scars
fibrillar

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19
Q

Col II

A

articular and hyaline cartilage

fibrillar

20
Q

Col III

A
  • embryonic collagen
  • in adults, found in bv, uterus, and GI tract
  • 1st collagen deposited in wound healing; eventually degraded and replaced by Col I
  • fibrillar
21
Q

Col IV

A

Basement membrane

Non-fibrillar (sheet)

22
Q

Elastic fibers

A
  • core of elastin surrounded by fibrillin
  • specialized fiber that allows for recoil after stretching
  • found in arteries, skin, uterus, lung
  • Marfans-mutation in fibrillin-aortic dissection, corneal dislocation, tall stature
23
Q

fibronectin

A
  • secreted cell adhesion protein
  • in plasma-stabilizes early clot (fibrin plug)
  • in cells (secreted from fibroblasts, macrophages, endothelial cells)
  • binds numerous molecules
  • first ECM deposited in wound healing
24
Q

functions of fibronectin

A
  • adds structural integrity to clot
  • chemotactic for many cells
  • substrate for cellular adhesion (RGD dominant)
  • substrate for other ECM protein attachment and assembly
25
Q

laminin

A
  • secreted cell adhesion protein
  • found primarily in BM-forms tight polymer networks w/ Col IV to maintain BM integrity
  • similar fxns to fibronectin: substrate for ECM protein binding and cell adhesion
26
Q

Integrins

A
  • cell surface bound adhesion protein
  • transmembrane receptors
  • facilitate cell-cell interaction
  • facilitate cellular interaction w/ ECM by binding collagen, fibronectin, and laminin
  • links cell surface to cytoskeleton-conformation changes may -> cell proliferation, apoptosis, differentiation, etc
27
Q

cadherins

A
  • cell surface bound adhesion protein
  • facilitate cell-cell interactions between similar cell types
  • facilitate formation of cell jxns
  • linked to cytoskeleton through catenins to regulate cell motility, proliferation, and differentiation
28
Q

proteoglycans

A
  • repeating polymers of disaccharides bound to a protein core
  • forms an ECM scaffold for tissue structure and permeability
29
Q

Hyaluronic acid

A
  • huge molecule of long repeating polysaccharides w/o a protein core
  • can bind large amount of H20-forms viscous hydrated gel; allows ECM to resist compressive forces, deposited early during wound healing to facilitate cell migration and proliferation
30
Q

Hemostasis phase of wound healing

A
  • 1st phase
  • stop bleeding and facilitate inflammation
  • platelets activated by exposed collagen
  • serum fibrin/fibronectin forms plug
  • platelets release thromboxane
  • vasodilation and increased permeability
31
Q

Inflammatory phase of wound healing

A
  • 2nd phase

- stop infection, clear debris, induce repair

32
Q

early inflammatory phase

A
  • neutrophils come (attracted by chemokines) -> phagocytosis

- Macrophages come -> predominate, secrete stuff, phagocytosis; orchestrate wound healing

33
Q

late inflammatory phase

A
  • macrophage secretion peaks
  • secreted factors attract and activate cells needed for proliferative phase
  • neutrophils and macrophages decrease
  • fibroblasts predominate
  • early wound ECM consists of fibrin, fibronectin, and HA-anchor for cell adhesion and collagen deposition
34
Q

Proliferative phase of wound healing

A
  • 3rd phase
  • replacement of lost tissue with scar
  • provides structural support
  • consists of: angiogenesis, formulation of granulation tissue, fibroplasia, epithelialization, wound contraction
  • fibroblast activity, ECM deposition, tissue remodeling
35
Q

Angiogenesis

A
  • restore perfusion to wound
  • VEGF -> increase vascular permeability, endothelial cell migration, promote angiogenesis
  • fibronectin/fibrin in ECM facilitate endothelial cell migration; proteases degrade existing ECM
  • new thin walled vessels in wound site
  • most vessels regress
36
Q

Granulation tissue

A
  • fills defects left by injury prior to vigorous collagen deposition
  • 2-5 days after injury
  • highly vascular loose fibrous tissue w/ scattered inflammatory cells and fibroblasts
  • ECM-fibronectin, Col III, HA
  • growth factors- PDGF and TGF-B
37
Q

Fibroplasia

A
  • influx and proliferation of fibroblasts w/ subsequent collagen deposition
  • fibroblasts attracted and activated by TFG-B, PDGF, EGF, FGF, and cytokines
  • 2-4 weeks
38
Q

TGF-B in fibrogenesis

A
  • increase fibroblast proliferation/migration
  • increase Col and fibronectin synthesis
  • decrease ECM degradation
  • chemotactic for monocytes
39
Q

Epithelialization

A
  • restoration of injured epithelium
  • basal keratinocytes proliferate from edges of wound-migrate in
  • stimulated by EGF, KGF, FGF
  • migration facilitated by interaction w/ fibronectin/fibrin in provisional ECM of granulation tissue (migrate over gran tissue and under scab)
40
Q

Contraction

A
  • pulls edges of wound together to reduce the wound surface area
  • decrease wound size by 40-80%
  • mediated by myofibroblasts
  • TGF-B induces differentiation of fibroblasts and myofibroblasts
  • myofibroblasts contain actin filaments that are linked to ECM and facilitate contraction
41
Q

Maturatoin phase

A
  • remodeling of ECM w/ mature scar formation to increase tensile strength
  • collagen production = degradation
  • can last over a year
  • matrix metalloproteinase degrade collagen and ECM
  • replace Col III w/ Col I -organized, cross linked, aligned along lines of tension (final strength 80%)
  • replace HA w/ proteoglycans
  • mature scar- dense Col I, elastic fibers, proteoglycans, scattered fibroblasts
42
Q

Local factors that affect wound healing

A
  • size, type, location of wound
  • vascular supply
  • oxygen supply
  • infection
  • necrosis-lowers tissue pH, causes inflammation, prevents healing
  • foreign material
  • movement
  • radiation
43
Q

Systemic factors that affect wound healing

A
  • circulatory compromise
  • nutritional status (protein, zinc, vit C, A, thiamine and riboflavin)
  • diabetes
  • obesity
  • hormones
  • chemotherapy
44
Q

Fibrosis

A
  • persistent stimulus (chronic inflammation) -> chronic activation of macrophages and lymphocytes
  • proliferation of fibroblasts, endothelial cells, and specialized fibrogenic cells; increase collagen synthesis, decrease collagen degradation
45
Q

healing by primary intention

A

-clean edges, close w/ stitches, glue, staples, etc

46
Q

healing by delayed primary intention

A

-wound is initially left open, when granulation tissue is judged clean and viable wound is closed by primary intention

47
Q

secondary intention

A
  • considered for contaminated or necrotic wounds, left open to scar in from below
  • greater inflammatory response, more granulation tissue, increased wound contraction, often larger scar

FM 1 (9 decks)

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