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Modulation of Microvascular Smooth Muscle Adhesion and Mechanotransduction by Integrin‐Linked Kinase
Author(s) -
HUANG SHAOXING,
SUN ZHE,
LI ZHAOHUI,
MARTINEZLEMUS LUIS A.,
MEININGER GERALD A.
Publication year - 2010
Publication title -
microcirculation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.793
H-Index - 83
eISSN - 1549-8719
pISSN - 1073-9688
DOI - 10.1111/j.1549-8719.2009.00011.x
Subject(s) - mechanotransduction , microbiology and biotechnology , integrin , chemistry , integrin linked kinase , kinase , biology , protein kinase a , receptor , biochemistry , cyclin dependent kinase 2
Microcirculation (2010) 17 , 1–15. doi: 10.1111/j.1549‐8719.2010.00011.x Abstract Objective: In this study, we investigated the involvement of integrin‐linked kinase (ILK) in the adhesion of arteriolar vascular smooth muscle cells (VSMC) to fibronectin (FN) and in the mechano‐responsiveness of VSMC focal adhesions (FA). Methods: ILK was visualized in VSMC by expressing EGFP–ILK and it was knocked down using ILK‐shRNA constructs. Atomic force microscopy (AFM) was used to characterize VSMC interactions with FN, VSMC stiffness and to apply and measure forces at a VSMC single FA site. Results: ILK was localized to FA and silencing ILK promoted cell spreading, enhanced cell adhesion, reduced cell proliferation and reduced downstream phosphorylation of GSK‐3β and PKB/Akt. AFM studies demonstrated that silencing ILK enhanced α5β1 integrin adhesion to FN and enhanced VSMC contraction in response to a pulling force applied at the level of a single FN–FA site. Conclusions: ILK functions in arteriolar VSMC appear linked to multiple signaling pathways and processes that inhibit cell spreading, cell adhesion, FA formation, adhesion to FN and the mechano‐responsiveness of FN–FA sites.