Wound Healing Flashcards
Regeneration
Renewal or compensatory growth to replace damaged tissues
Repair
Fibrous scar production (fibrosis) to patch damaged tissue
Permanent cells
Unable to regenerate e.g. neutrons, cardiac monocytes
Labile cells
Divide in homeostasis - rapid regeneration
In skin and GI tract as damage on outside means there is constant need for proliferation
Stable cells
Non proliferative in homeostasis but capable of regenerating after injury e.g. liver, kidney
Regenerative signals after injury - physical stimuli
Cell-cell interactions
cell-matrix interactions (mediated by integrins which trigger intracellular cascades)
Regenerative signals after injury - soluble growth factors
Paracrine signalling - leave cell and act on the cells in the local area
Endocrine - release soluble factors into the blood stream and act on other cells further away
Autocrine - leave cell and act on cell surface receptors of the same cell
Scar formation
Fibroblast migration and proliferation -> extracellular matrix deposition -> tissue remodelling
Fibroblasts
Migration and proliferation is triggered by growth factors (e.g. TGI beta)
Lay down more matrix and prevent breakdown by producing TIMPS
Source of connective tissue
Resident mesenchymal cells
Responsible for scarring - non polar so can grow in any direction
ECM deposition
Produced by fibroblasts
Collagens type I/III (fibrillar) and IV (basement membrane type)
Elastics, proteoglycans, glycoproteins
Net fibrillar collagen productions increased and degradations decreased
Tissue remodelling
Mediate long term scar maturation and degradation
Remodelling of granulation tissue ECM requires degranulation by matrix metalloproteinases (MMPs)
Highly regulated by Tissue inhibitors of mertalloproteinases (TIMPs)
