Epidermal Growth Factor

• EGFR1 mutations in Head, neck, breast, lung cancers

Transforming growth factor(TGF-α)

ERB b2 receptor(HER2)

• Transforming growth factor(TGF-α)
• ERB B2 receptor (HER2) overexpressed in breast cancer

Vascular Endothelial GF(VEGF)

• Vasculogensis and Angiogenesis

TGF-β

(Transforming GF)

TGF-β

• Growth inhibitor for most epithelial cells

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• Fibrogenic agent -> Fibrosis
• Fibroblast migration/replication

• Strong anti-inflammatory effect

Healing by repair, Scar formation and fibrosis

(Damge to what prevents healin?)

(What is healing?)

Healing by repair, Scar formation and fibrosis

• Healing not possible if Severe damage to parenchymal and Stromal framework 

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• Main healing is repair by deposition of collagen and other ECM components creating a scar

DLL4/Notch

• Decrease: sprouting, EC proliferation,
• Increases: Vessel lumen size, Vascular organization

VEGF/VEGFR

• Increase: Sprouting, EC proliferation, EC survival
• Decrease: Vascular organization

Clot formation

Clot Formation

• Clot formation from Rapid activatio nof coagulation pathways; contains fibrin, fibronectin, complement.

• Clot stops bleeding and serves as scaffold for migrating cells

• Within 24 hours neutrophils use clot as scaffold and clean out debris/bacteria via proteolytic enzymes

Recovery of Tensile Strength

Fibrillar collagens(Type I) form major portion of CT in repair sites.

In 3 months 70 to 80% is the max tensile strength recovered from collagen deposition and cross-linking

Primary Union

• Thin wound, small clot No scar formation
• Epithelial cells can grow form side to side

Secondary Union

• Scar formation, wound contraction(myofibroblats contract to bring wound together)
•  Granulation tissue

Pathologic aspects of repair

Keloid?

Keloid

• Excess granulation tissue, if cut just grows back
• More prevalent in african and americans

TGF-β and fibrosis

• TGF-β is always involved as an important fibrogenic agent
• TGF-β is important for collagen deposition