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Editorial
. 2010 Apr 2;106(6):1014-6.
doi: 10.1161/CIRCRESAHA.110.217786.

Regulation of myoendothelial junction formation: bridging the gap

Steven S Segal, Pooneh Bagher
Editorial

Regulation of myoendothelial junction formation: bridging the gap

Steven S Segal et al. Circ Res. .
No abstract available

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Conflict of interest statement

Conflict of interest disclosures: None

Figures

Figure 1
Figure 1. Plasminogen activator inhibitor-1 (PAI-1) regulates myoendothelial junction (MEJ) formation
According to new findings presented by Heberlein and co-workers , MEJ formation is regulated through PAI-1 actions on the plasminogen activator (PA) system. A. Flow diagram indicating how PAI-1 levels determine whether plasminogen activators (t-PA and u-PA) are able to convert plasminogen (inactive zymogen) into plasmin (active protease). A reduction in PAI-1 elevates plasmin concentration (right), thereby increasing matrix degradation, reducing cell adhesion and diminishing MEJ formation. Conversely, an increase in PAI-1 (left) reduces plasmin production, thereby decreasing matrix degradation, enhancing cell adhesion and increasing MEJ formation. B. Illustration of a MEJ between an EC and VSMC in the presence of PAI-1 (black circles). Translocation of exogenous PAI-1 from the apical surface of EC to the MEJ (but not from the apical surface of VSMC) was found to promote MEJ formation in VCCC. These observations raise several new questions about the mechanism of action of PAI-1: (1) What receptor(s) or transporter(s) does PAI-1 act on at the apical membrane of EC? (2) How is PAI-1 transported from the plasma membrane of EC to the MEJ? (3) What additional signaling events (e.g., transcriptional regulation of proteins localized to MEJs) are activated by PAI-1 within EC to promote MEJ formation? (4) How does PAI-1 promote invasion of the ECM and the IEL in forming a new MEJ? While VSMC apparently bind PAI-1 at their apical surface they do not translocate it to the MEJ, leading to the question: (5) What intracellular transport machinery is lacking in VSMC that prevents these cells from trafficking PAI-1 to the MEJ?
See this image and copyright information in PMC

Comment on

References

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    1. Isakson BE, Duling BR. Heterocellular contact at the myoendothelial junction influences gap junction organization. Circ Res. 2005;97(1):44–51. - PubMed

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