Emt types i and ii

FACTORS TRIGGERING EMT: Possibility of EMT type I in adults overpassing EMT type II and the inherent inflammation
We have three types of epithelial-mesenchymal transition: type I is associated with embryologic development, type II with inflammatory response and type III occurs in epithelial cancer cells.
Being our goal the heart tissue regeneration, type II EMT which is an answer to tissue inflammation is not suitable. Type I on the other hand could be our solution because it is involved in all tissue formation. * Factors triggering EMT type I and type II * Growth factors and cytokines: TGFb, EGF, HGF, FGF * ECM components through integrins * Wnt proteins, Notch * Hypoxia (HIF) - regulates cellular adaptation to changes in oxygen tension * ROS (superoxide, hydroxyl radical and hydrogen peroxide)- function as a second messenger in signal transduction pathways for a variety of cellular processes, including proliferation, differentiation, and migration. * Mechanical stress- FAK may mediate the transmission of mechanical stress into biochemical signals. * Type 1 * Growth factors and cytokines: TGFb, EGF, HGF, FGF * FGF (witch receptor is FGFR1) - regulates migration and patterning of mesoderm at gastrulation, differentiate epithelial cells to myofibroblasts and cause organ fibrosis, promotes proliferation of many cells; inhibits some stem cells; induces mesoderm to form in early embryos. * The HGF receptor (Met)- regulates the Snail expression and affect the localization of adherens and tight junction proteins. * EGF receptor family (EGFR, ErbB, or HER) - represses E-cadherin by promoting its endocytosis and also by inducing the expression of Snail and Twist. * -TGF-β- anti-inflammatory (suppresses cytokine production and class II MHC expression), promotes wound healing, inhibits macrophage and lymphocyte proliferation. * TGF-β/Nodal and Vg1)- mediate the action of Wnt. * Wnt- is associated with