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Endothelial IQGAP1 regulates efficient lymphocyte transendothelial migration.

Maryam Nakhaei-Nejad¹, Qiu-Xia Zhang, Allan G Murray

¹Department of Medicine, University of Alberta, Edmonton, Alberta, Canada.

European Journal of Immunology

|December 18, 2009

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IQGAP1 stabilizes microtubules at endothelial junctions, crucial for lymphocyte transendothelial migration. This protein is vital for efficient leukocyte diapedesis during inflammation, independent of cell junction gaps.

Area of Science:

Cell Biology
Immunology
Inflammation Research

Background:

Leukocyte extravasation is key in inflammatory diseases.
Endothelial cell (EC) roles in leukocyte recruitment are known, but junction remodeling mechanisms during transendothelial migration (TEM) are unclear.

Purpose of the Study:

Investigate the role of IQGAP1 in lymphocyte TEM.
Determine IQGAP1's contribution to EC shape and adhesive contacts during leukocyte migration.

Main Methods:

Studied IQGAP1 in endothelial cells (ECs) using knockdown techniques.
Utilized nocodazole treatment to depolymerize microtubules (MTs).
Employed confocal microscopy to image lymphocyte TEM and VE-cadherin junctions.

Main Results:

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EC IQGAP1 knockdown reduced lymphocyte TEM by ~70% and decreased MT tethering at adherens junctions.
Nocodazole-induced MT loss decreased lymphocyte TEM by ~65%.
Both interventions caused lymphocyte accumulation at junctions and reduced diapedesis, without affecting VE-cadherin gap formation.

Conclusions:

IQGAP1 stabilizes endothelial MTs at interendothelial junctions.
IQGAP1 is essential for efficient lymphocyte diapedesis, independent of VE-cadherin gap formation.
Findings elucidate novel mechanisms in leukocyte recruitment during inflammation.