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The efficiency of growth factors on the nanofibrous matrix to activate signaling molecules was studied in HUVECs through gene expression analysis.
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Bone healing requires both resident cells and endogenous bioactive molecules that are locally produced or brought into the circulation to the extracellular matrix (ECM) to activate the cascade of repair [ 6– 17].
Fibrin-based matrices appear to activate angiogenic signaling in ASCs while P-fibrin matrices are uniquely able to also drive a vessel-like ASC phenotype.
In this paper, the operational times are modeled and introduced into the matrix system model to activate the matrix system functioning.
Mitochondria behave as a percolation matrix: to be activated, mitochondria have to be near threshold, which could explain the fact that some neighboring mitochondria are devoid of flashes [32].
uPA converts plasminogen into the active serine protease plasmin, a broad spectrum protease that can degrade many different types of extracellular matrix proteins in addition to activate latent growth factors and matrix metalloproteases [ 24, 25].
Furthermore, both the integrin av β6 and active matrix metalloproteinase-2, known to activate TGF- β, are associated with poor disease-specific survival (Sier et al, 2006; Hazelbag et al, 2007).
Using the well-defined matrix as a tool to activate integrins α5β1 plus αvβ5, α6β1 and α9β1, individually and in combination, differential integrin activation was demonstrated to exert exquisite control over ESC fate decisions.
In a functional proteomic screen for proteins required for invasion, extracellular heat shock protein 90 alpha (Hsp90α) was identified and shown to activate matrix metalloproteinase 2 (MMP-2).
TGF-β1 has also been shown to activate matrix production in articular chondrocytes via ERK1/2 [ 50].
Extracellular HSP90 has also been shown to activate matrix metalloproteinase-2 [ 28] and plasminogen [ 54] leading to increased cell motility.
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