Cortactin deficiency is associated with reduced neutrophil recruitment but increased vascular permeability in vivo

Abstract

Cortactin is required for endothelial barrier function and leukocyte recruitment in vivo.

Microtubule Dynamic Instability Controls Podosome Patterning in Osteoclasts through EB1, Cortactin, and Src

“…siRNA-mediated knockdown of cortactin in fibroblasts (85), smooth muscle cells (86), tumor cells (51,(87)(88)(89)(90), or OCs (52, 53) prevents the formation of podosome and invadopodia. To determine which role cortactin plays in podosome patterning and belt formation, we used OCs derived from cortactin knockout mice (36). In contrast to previous reports, we found that cortactin is dispensable for podosome formation in OCs.…”

FGF23 signaling impairs neutrophil recruitment and host defense during CKD

“…Transendothelial migration of isolated murine neutrophils though a bEnd.5 endothelial cell monolayer was analyzed as described before (58).…”

Dynamics between actin and the VE-cadherin/catenin complex

“…[68][69][70][71][72][73][74][75][76] Importantly, recent data indicates the involvement of p120 ctn in controlling ARP2/3 complex-mediated actin polymerization at endothelial junctions, by binding to the nuclear-promoting factors Wiskott-Aldrich Syndrome Protein (N-WASP) 21 and to cortactin. 77,78 Both the ARP2/3 complex 11,21 and cortactin [79][80][81][82][83][84][85] control endothelial integrity, and particularly, N-WASP control ARP2/3 complex-mediated formation of new VE-cadherin adhesion sites, which drive the VE-cadherin dynamics.…”

“…Another protein that controls the ARP2/3 complex activity is cortactin, a class II NPF that has been demonstrated to control endothelial barrier function and leucocyte transmigration. 79,80,83,85,99,100 Furthermore, cortactin has multiple functions in cell motility and is able to activate N-WASP. 101 For further readings to cortactin, please see recent reviews.…”

“…Those cells displayed less JAIL, less VE-cadherin dynamics, and dramatically reduced the overall cell motility within the endothelial monolayer 11 (link: http://www.molbiolcell.org/content/suppl/2013/11/11/ mbc.E13-07-0404v1.DC1/mc-E13-07-0404-s06.mp4), while inhibition of ARP2/3 complex blocked VE-cadherin dynamics and caused intercellular gap formation. 11 Gap formation was also demonstrated using N-WASP mutants 11,21 or depletion of cortactin, 85 molecules that to the end control the activity of the ARP2/3 complex. 113,114 Although the molecular mechanisms that control interaction between JAIL formation and VE-cadherin-mediated cell adhesion is incompletely understood there is evidence that α-catenin and p120 ctn , components of the VE-cadherin/catenin complex, are interaction partners for molecules that control actin polymerization.…”