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Related Concept Videos

Cell Migration01:19

Cell Migration

Cell migration is a process by which the cells move from one location to another, playing an essential role in embryological development, repair and regeneration, immune response, and metastasis. Cells migrate in response to chemical or mechanical signals generated by specific organs or tissues. The overall mechanism includes three steps - polarization, protrusion, and release. Polarization involves the formation of a distinct cell front and rear, which determines the direction of movement.
Cell Migration01:09

Cell Migration

Cell migration, the process by which cells move from one location to another, is essential for the proper development and viability of organisms throughout their life. When cells are not able to migrate properly to their ordained locations, various disorders may occur. For example, disruption in cell migration causes chronic inflammatory diseases such as arthritis.
Introduction to Fibroblasts01:09

Introduction to Fibroblasts

Rudolph Virchow discovered spindle-shaped cells called fibroblasts in 1858. Inactive fibroblasts, called fibrocytes, become activated by various stimuli, such as growth factors and inflammatory cytokines. Activated fibroblasts play a crucial role in wound healing, inflammation, formation of new blood vessels, and cancer progression. Uncontrolled activation of fibroblasts results in fibrosis, the excess deposition of fibrous tissue, which can lead to scarring and affect normal organs. This...
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TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
Activation of Integrins01:15

Activation of Integrins

Integrins bind ligands and transmit information from outside the cell to inside or vice-versa through an "outside-in signaling" or "inside-out signaling."
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Fibroblast migration is mediated by CD44-dependent TGF beta activation.

Pinak S Acharya1, Sonali Majumdar, Michele Jacob

  • 1Department of Pulmonary and Critical Care Medicine, The University of Pennsylvania, Philadelphia, PA 19104, USA.

Journal of Cell Science
|April 10, 2008
PubMed
Summary

CD44 deficiency in fibroblasts impairs wound healing by affecting cell migration and tissue remodeling. CD44 is crucial for fibroblast recruitment and activation of TGF-beta, impacting inflammation and fibrosis.

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Area of Science:

  • Cell Biology
  • Biochemistry
  • Immunology

Background:

  • CD44 plays a role in inflammation and fibrosis following tissue injury.
  • Fibroblast recruitment is essential for effective wound healing and tissue repair.

Purpose of the Study:

  • To investigate the role of CD44 in fibroblast cytoskeletal architecture and migration.
  • To elucidate the mechanisms by which CD44 influences fibroblast behavior, including TGF-beta activation.

Main Methods:

  • Comparison of wild-type (CD44WT) and CD44-deficient (CD44KO) fibroblasts.
  • Analysis of cytoskeletal structure, focal adhesions, and cell migration patterns.
  • Assessment of active TGF-beta production and matrix metalloproteinase (MMP) activity.

Main Results:

  • CD44KO fibroblasts showed reduced stress fibers and focal adhesions, with faster but less directed migration.
  • CD44WT cells produced more active TGF-beta than CD44KO cells, mediated by MMPs.
  • Restoring CD44 expression rescued fibroblast phenotype; active TGF-beta partially rescued defects but not directionality.

Conclusions:

  • CD44 is critical for fibroblast migration directionality and TGF-beta activation.
  • CD44 influences both TGF-beta-dependent and independent pathways in fibroblast function.
  • CD44 is vital for fibroblast recruitment, tissue remodeling, and fibrosis in response to injury.