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Impact of cyclic strain on integrin expression in rat pulmonary microvascular endothelial cells
Author(s) -
Villalta Patricia Caridad,
Rocic Petra,
Townsley Mary I.
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.797.1
Subject(s) - integrin , extracellular matrix , microbiology and biotechnology , strain (injury) , collagen receptor , matrix (chemical analysis) , chemistry , basement membrane , biophysics , biology , cell , anatomy , biochemistry , chromatography
Detachment of pulmonary microvascular endothelial cells (PMVEC) is observed in mechanical stress‐induced, TRPV4‐mediated (vanilloid transient receptor potential 4 channel) acute lung injury. Integrin dimers, comprised of α and β subunits, that mediate PMVEC tethering and detachment have not been identified. The goals of this study were to characterize integrin expression and to identify the effect of cyclic strain on integrin expression. Rat PMVEC were cultured on collagen I or pronectin flexwell membranes to 90% confluence and then subjected to 0% or 10% uniaxial strain at 30 cycles/min for 24 h. Using PCR and primers for rat integrins, expression of integrin subunits α1, α2, α3, α5, α6, α7, αv, β1, and β6, but not α4, α8 or β3, was identified in PMVEC, irrespective of strain or matrix composition. However, integrin β4 expression decreased with cyclic strain in PMVEC cultured on either matrix. Based on these results, extracellular ligands for integrin dimers, and matrix composition of the alveolar basement membrane, we predict that α1β1, α2β1, α3β1, α6β1, α7β1, and/or α6β4 could tether PMVEC to matrix in vivo and be a target for detachment in TRPV4‐mediated acute lung injury. Supported by HL066299 and HL076125.