Role of cell adhesions in neural development: Difference between revisions

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Cellular adhesions can be defined as proteins or protein aggregates that form mechanical and chemical linkages between the intracellular and extracellular space. Adhesions serve several critical processes including cell migration, signal transduction, tissue development and repair. Due to this functionality, adhesions and adhesion molecules have been a topic of study within the scientific community. Specifically, it has been found that adhesions are involved in tissue development, plasticity, and memory formation within the central nervous system (CNS), and may prove vital in the generation of CNS-specific therapeutics.

[[File:Adhesion_diagramAdhesion diagram.jpg|thumb|alt=A | Image courtesy of wikipedia user JWSchmidt under the GNU Free Documentation License]]

==Adhesion classifications==

* '''Cell-cell adhesions''' provide chemical and mechanical connections between adjacent cells. Of special importance to neuronal tissue development are the subcategory [[CDH2|n-cadherins]]. These cadherin molecules have been shown to be important in formation of the CNS structure, as well as neuronal migration along glial fibers.<ref>{{cite journal|last=Murase|first=S|title=The role of cell adhesion molecules in synaptic plasticity and memory.|journal=Current Opinion in Cell Biology|year=1999|month=Oct|volume=11|issue=5|pages=549-53549–53}}</ref>

* '''Cell-'''[[Extracellular matrix|'''Extra-Cellular Matrix''']] (ECM) '''adhesions''' also form mechanical and chemical linkages, but the connection occurs between cellular-matrix and the extra-cellular matrix through a plethora of adhesive proteins that form cohesive functional units. These focal adhesion plaques are highly dynamic in nature and undergo a maturation process through which they have altered functionality and protein content. Maturation stages are summarized in the following table:

{| class="wikitable sortable"

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===Thy-1 adhesion protein===

Thy-1 (or [[thy-1|CD90.2]]) is a membrane bound [[glycoprotein|glycoprotein]] that has been shown to be involved in the [[axon guidance|axon guidance]] pathway. This protein has been shown to be highly mobile, as it contains a [[Glycophosphatidylinositol|GPI]] membrane anchor. Although much of the details are elusive, it is known that thy-1 interacts with the protein dimer integrin found on [[astrocytes|astrocytes]], forming aggregates that can inhibit neurite outgrowth and extension. Thy-1 has also been shown to have involvement in the [[src (gene)|src]]-family kinase pathway.<ref>{{cite journal|last=Rege|first=Tanya|title=Thy-1, via its GPI anchor, modulates Src family kinase and focal adhesion kinase phosphorylation and subcellular localization, and fibroblast migration, in response to thrombospondin-1/hep I|journal=Chronology|year=2006|doi=10.1016/j.yexcr.2006.07.029}}</ref> This astrocyte-neuron feedback has been proposed as a mechanism involved in CNS tissue repair post-injury, as a down regulation of thy-1 may lead to enhanced neurite outgrowth. Additional research has shown that thy-1 expression in post natal humans is elevated for several weeks. This suggests that in addition to tissue repair, thy-1 might have roles in early CNS tissue development and organization.<ref>{{cite journal|last=Herrera-Molina|first=Rodrigo|coauthors=et al|title=Astrocytic aVb3 Integrin Inhibits Neurite Outgrowth and Promotes Retraction of Neuronal Processes by Clustering Thy-1|journal=PLos ONE|year=2012|month=May|volume=7|series=3|pages=e34295}}</ref><ref>{{cite journal|last=Barker|first=Thomas|title=Thy-1 regulates fibroblast focal adhesions, cytoskeletal organization and migration through modulation of p190 RhoGAP and Rho GTPase activity|journal=Experimental Cell Research|year=2004|issue=295|pages=488–496}}</ref>

===L1 family protein===

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Several debilitating diseases are brought about from errors in neural development due in part to problems involving neural cell adhesions and adhesion mechanisms.

*CRASH syndrome (or L1 syndrome) is brought about by a mutation in the L1CAM gene on the x-[[chromosome|chromosome]], resulting in a malfunctioning L1CAM protein. CRASH (acronym) syndrome include the conditions:<ref name="pmid8556302">{{cite journal |author=Fransen E, Lemmon V, Van Camp G, Vits L, Coucke P, Willems PJ |title=CRASH syndrome: clinical spectrum of corpus callosum hypoplasia, retardation, adducted thumbs, spastic paraparesis and hydrocephalus due to mutations in one single gene, L1 |journal=European Journal of Human Genetics |volume=3 |issue=5 |pages=273–84 |year=1995 |pmid=8556302 }}</ref>

{| class="wikitable"<ref name="pmid7562969">{{cite journal |author=Ruiz JC, Cuppens H, Legius E, ''et al.''|title=Mutations in L1-CAM in two families with X linked complicated spastic paraplegia, MASA syndrome, and HSAS |journal=Journal of medical genetics |volume=32 |issue=7 |pages=549–52 |year=1995 |month=July |pmid=7562969 |pmc=1050549 |doi= 10.1136/jmg.32.7.549|url=}}</ref>

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|row5=[[Hydrocephalus]] {{!!}} Abnormal accumulations of [[Cerebrospinal fluid]] within skull}}

*Additionally, studies have shown that alterations in the expression of the protein thy-1 may be partially responsible for the abnormal neuronal outgrowth observed in [[Alzheimer's]] patients. It was found that abnormal neural outgrowth and thy-1 presence were correlated spatially, though mechanistic work is still needed to better understand thy-1's involvement in this condition.<ref>{{cite journal|last=Leifer|first=D|title=Thy-1 in hippocampus: normal anatomy and neuritic growth in Alzheimer's disease.|journal=Journal of Neuropathology & Experimental Neurology|year=1992|month=March|volume=51|issue=2|pages=133-41133–41}}</ref>

==References==

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{{Reflist}}

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[[Category:Biology]]

[[Category:Neuroscience]]