Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2013 May 15;319(9):1247-54.
doi: 10.1016/j.yexcr.2013.03.028. Epub 2013 Apr 6.

Polarizing pathways: balancing endothelial polarity, permeability, and lumen formation

Affiliations
Review

Polarizing pathways: balancing endothelial polarity, permeability, and lumen formation

Carlos O Lizama et al. Exp Cell Res. .
No abstract available

PubMed Disclaimer

Figures

Figure 1
Figure 1
Balancing migration and cell-cell adhesion. In response to growth factor cues (in this example VEGF, pink), the migratory endothelial cell will orient filopodia and lamellipodia to the leading front while the cell undergoes cytoskeletal rearrangement. Caveolin1 interacts with 31 integrin as the cell migrates, and participates in the endocytosis and recycling of integrins. In response to polarity and matrix cues, RhoA is initiated at the site of protrusion and actin assembly. Cdc42 and Rac1 function to propagate the initiating event. Amot and AmotL1 interact with Syx (and can interact with each other) to regulate RhoA both at the cell-cell tight junctions (TJ) and in the polarized leading edge. Phosphorylated VEGFR2 (pVEGFR) is co-trafficked with Amot and Syx and function in TJ disassembly. TJ is represented by Occludin, ZO-1 and VE-cadherin.
Figure 2
Figure 2
Lumen formation within the aorta. The contact sites of neighboring endothelial cells are comprised of junctional proteins, one of which is VE-cadherin. VE-cadherin can associate with both CCM-1 and Par3 proteins, which regulate apical/basal polarity and lumen formation. As the luminal membrane becomes polarized, apical localization of sialomucins (CD34 and podocalyxin) is noted. Negatively charged sialomucins cause membrane repulsion, as moesin associates with CD34 and recruits F-actin, and eventually nm myosin II, to the apical membrane. This actin/myosin recruitment and assembly generates contractile forces that regulate cell shape changes resulting in a patent lumen. β1 integrin is located in the basolateral membrane has been demonstrated to also play a role in cell shape and lumen formation, possibly by acting to counterbalance apical forces in the process.

Similar articles

Cited by

References

    1. Simons M, Mlodzik M. Planar cell polarity signaling: from fly development to human disease. Annu Rev Genet. 2008;42:517–40. - PMC - PubMed
    1. Wehrle-Haller B, Imhof BA. Actin, microtubules and focal adhesion dynamics during cell migration. Int J Biochem Cell Biol. 2003 Jan;35(1):39–50. - PubMed
    1. Lamalice L, Le Boeuf F, Huot J. Endothelial cell migration during angiogenesis. Circulation Research. 2007 Mar 30;100(6):782–94. - PubMed
    1. Gerhardt H, Golding M, Fruttiger M, Ruhrberg C, Lundkvist A, Abramsson A, et al. VEGF guides angiogenic sprouting utilizing endothelial tip cell filopodia. The Journal of Cell Biology. 2003 Jun 23;161(6):1163–77. - PMC - PubMed
    1. Parker KK, Brock AL, Brangwynne C, Mannix RJ, Wang N, Ostuni E, et al. Directional control of lamellipodia extension by constraining cell shape and orienting cell tractional forces. FASEB J. 2002 Aug;16(10):1195–204. - PubMed