Cardiac neural crest: Difference between revisions

Revision as of 13:05, 13 August 2013

Revision as of 11:50, 14 August 2013

Line 33:

=== Migration into the Cardiac Outflow and Proximal Outflow ===

The cardiac outflow tract is a temporary structure in a developing embryo that connects the [[ventricle]]sventricles with the [[aortic sac]].<ref name="gilbert" /><ref name="kur" /> Some cells further migrate to the cardiac outflow instead of the pharyngeal arches.<ref name="kirby1987" /><ref name="kur" /><ref name="kirby2010" /> The cardiac neural crest in the outflow tract creates cardiac [[Ganglion

|ganglia]] and [[mesenchyme]] at the junction of the subaortic and sub pulmonary myocardium (muscular heart tissue) of the outflow tract.<ref name="kirby2010" /> A small amount of CNCCs also migrates further into the proximal outflow tract where they help to close the ventricular outflow septum.<ref name="kirby1987" /><ref name="kur" />

Line 42:

=== Wnt ===

Wnt proteins are extracellular growth factors that activate different intracellular signaling branches.<ref name="gessert">{{cite journal|last=Gessert|first=S|coauthors=Kuhl M|title=The multiple phases and faces of wnt signaling during cardiac differentiation and development.|journal=Circulation Research|year=2010|volume=107|pages=186–199|doi=10.1161/CIRCRESAHA.110.221531|url=http://circres.ahajournals.org/content/107/2/186.full|accessdate=19 November 2012|issue=2}}</ref> There are 2 types of pathways: canonical and non-canonical.<ref name="gessert" /> The classic canonical Wnt pathway involves [[Beta-catenin|B-catenin]] protein as a signaling mediator.<ref name="gessert" /> Wnt maintains B-catenin by preventing against [[Proteasome]] degradation.<ref name="gessert" /> Thus, B-catenin is stabilized in the presence of Wnt and regulates gene transcription through interaction with TCF/LEF transcription factors.<ref name="gessert" /> The canonical Wnt/B-catenin pathway is important for [[Proliferation|cell proliferation]] control.<ref name="kirby2010">{{cite journal|last=Kirby|first=ML|coauthors=Hutson MR|title=Factors controlling cardiac neural crest cell migration|journal=Cell adhesion and migration|year=2010|month=December|volume=4|issue=4|doi=http://dx.doi.org/10.4161/cam.4.4.13489|accessdate=20 November 2012}}</ref> The non-canonical Wnt pathway is independent of B-catenin and has an inhibitory effect on canonical Wnt signaling.<ref name="gessert" />

Wnt signaling pathways play a role in CNCC development as well as OFT development.<ref name="gessert" /> In mice, decrease of B-catenin results in a decrease in the proliferation of CNCCs.<ref name="gessert" /> Downregulation of the Wnt coreceptor Lrp6 leads to a reduction of CNCCs in the dorsal neural tube and in the pharyngeal arches, and results in ventricular, septal, and OFT defects.<ref name="gessert" /> Canonical Wnt signaling is especially important for cell cycle regulation of CNCC development and the initiation of CNCC migration.<ref name="gessert" /> Non-canonical Wnt signaling plays a greater role in promoting cardiac differentiation and OFT development.<ref name="gessert" />