Haptotaxis

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Haptotaxis (from Greek ἅπτω (hapto, "touch, fasten") and τάξις (taxis, "arrangement, order")) is the directional motility or outgrowth of cells, e.g. in the case of axonal outgrowth, usually up a gradient of cellular adhesion sites or substrate-bound chemoattractants (the gradient of the chemoattractant being expressed or bound on a surface, in contrast to the classical model of chemotaxis, in which the gradient develops in a soluble fluid.). These gradients are naturally present in the extracellular matrix (ECM) of the body during processes such as angiogenesis or artificially present in biomaterials where gradients are established by altering the concentration of adhesion sites on a polymer substrate.[1][2]

Clinical Significance.[edit]

Haptotaxis plays a major role in the efficient healing of wounds.[3][4] When corneal integrity is compromised epithelial cells quickly cover the damaged area by proliferation and migration(Haptotaxis). In the Stroma, Keratocytes within the wounded area undergo apoptosis leaving the stroma devoid of cells that must be replaced and the keratocytes surrounding the wounded area proliferate and become fibroblast that migrate to fill the stromal wounded area. This creates a healthy environment with myofibroblasts and ECM. This is known as light backscattering or subepithial haze.[5] When there is injury to an epithethial cells heptataxis occurs and this is highly influenced by the cells velocity . This velocity is influenced by direction of cell motility. Cells migrate easily and quickly in packs so when one cell moves, the rest follow in response to the gradient and initial cell movement. Mechanical effects like the buildup of tension in the may play an important role for both division as well as motility of cells in tissue.[6]

References[edit]

  1. ^ McCarthy JB, Palm SL, Furcht LT. (1983). "Migration by haptotaxis of a Schwann cell tumor line to the basement membrane glycoprotein laminin". J Cell Biol 97 (3): 772–7. doi:10.1083/jcb.97.3.772. PMC 2112555. PMID 6885918. 
  2. ^ Cattaruzza S, Perris R. (2005). "Proteoglycan control of cell movement during wound healing and cancer spreading". Matrix Biol 24 (6): 400–17. doi:10.1016/j.matbio.2005.06.005. PMID 16055321. 
  3. ^ Blanco-Mezquita, Jose; Hutcheon, Audrey E.K; Zieske, James D. (January 28, 2013). "Role of Thrombospondin-1 in Repair of Penetrating Corneal Wounds". Invest ophthalmology: 7. doi:10.1167/iovs.13-11710. 
  4. ^ Basan, Markus; Elgeti, Jens; Hannezo, Edouardo; Rappel, Wouter-Jan; Levine, Herbert (2012-09-09). "lignment of cellular motility forces with tissue flow as a mechanism for efficient wound healing". Proceedings of the National Academy of Sciences of the United States of America PNAS, Proceedings of the National Academy of Sciences (PNAS 2013 110:2452-2459): 8. Retrieved 6 November 2014. 
  5. ^ Blanco-Mezquita, Jose; Hutcheon, Audrey E.K; Zieske, James D. (January 28, 2013). "Role of Thrombospondin-1 in Repair of Penetrating Corneal Wounds". Invest ophthalmology: 7. doi:10.1167/iovs.13-11710. 
  6. ^ Basan, Markus; Elgeti, Jens; Hannezo, Edouardo; Rappel, Wouter-Jan; Levine, Herbert (2012-09-09). "lignment of cellular motility forces with tissue flow as a mechanism for efficient wound healing". Proceedings of the National Academy of Sciences of the United States of America PNAS, Proceedings of the National Academy of Sciences (PNAS 2013 110:2452-2459): 8. Retrieved 6 November 2014. 

External links[edit]

  • "Cellular Migration" - University of California, Berkeley, 2003. Cell and Tissue Engineering website.