| dc.description.abstract | Arterial aging is characterized by reduced vessel contractility, arterial stiffening and endothelial dysfunction which are major predictors of cardiovascular diseases present in the elder population. At the level of vascular smooth muscle cells, this corresponds to age-induced phenotypic changes from a contractile to a synthetic phenotype associated with decreased mechanosensitive responses to external stimuli in these cells. This study is focused on analyzing the integrin role as a contributor to arterial vasomotor dysfunction through the regulation of vascular smooth muscle cells adhesion to extracellular matrix components. To test the effects of matrix-functionalized substrate stiffness on integrin spatial distribution, vascular smooth muscle cells isolated from soleus feed arteries of young and old Fisher 344 rats were plated on glass-bottom cell culture dishes functionalized with matrix proteins, fibronectin and collagen I. Then, cells were stained for endogenous beta-1 integrin using mouse anti-beta-1-Alexa 488 direct-labeled antibody (Biolegend, San Diego, CA). Stained cells were imaged using total internal reflection fluorescence and confocal microscopy to analyze spatial distribution of beta-1 integrin at cell-matrix adhesions. Our results showed a significantly higher fluorescence intensity, indicating a greater amount of integrin beta-1 present at cell-matrix adhesions in young versus old vascular smooth muscle cells, in all conditions. The decrease of beta-1 integrin recruitment at cell-matrix adhesions in old cells, shows a reduced cell adhesion to the matrix that correlates well with the decreased contractility of aged vascular smooth muscle cells. The work presented here partially references the abstract accepted to the 65th Biophysical Society Meeting (Ojha et al 2021). | |
