35 research outputs found
Vascular Smooth Muscle Cell Stiffness and Adhesion to Collagen I Modified by Vasoactive Agonists
In vascular smooth muscle cells (VSMCs) integrin-mediated adhesion to extracellular
matrix (ECM) proteins play important roles in sustaining vascular tone and resistance.
The main goal of this study was to determine whether VSMCs adhesion to type I collagen
(COL-I) was altered in parallel with the changes in the VSMCs contractile state induced by
vasoconstrictors and vasodilators. VSMCs were isolated from rat cremaster skeletal muscle
arterioles and maintained in primary culture without passage. Cell adhesion and cell E-modulus
were assessed using atomic force microscopy (AFM) by repetitive nano-indentation of
the AFM probe on the cell surface at 0.1 Hz sampling frequency and 3200 nm Z-piezo travelling
distance (approach and retraction). AFM probes were tipped with a 5 μm diameter
microbead functionalized with COL-I (1mg\ml). Results showed that the vasoconstrictor angiotensin
II (ANG-II; 10−6
) significantly increased (p<0.05) VSMC E-modulus and adhesion
probability to COL-I by approximately 35% and 33%, respectively. In contrast, the vasodilator
adenosine (ADO; 10−4
) significantly decreased (p<0.05) VSMC E-modulus and adhesion
probability by approximately −33% and −17%, respectively. Similarly, the NO donor
(PANOate, 10−6 M), a potent vasodilator, also significantly decreased (p<0.05) the VSMC
E-modulus and COL-I adhesion probability by −38% and −35%, respectively. These observations
support the hypothesis that integrin-mediated VSMC adhesion to the ECM protein
COL-I is dynamically regulated in parallel with VSMC contractile activation. These data suggest
that the signal transduction pathways modulating VSMC contractile activation and relaxation,
in addition to ECM adhesion, interact during regulation of contractile state