I suppose that depends on how you define endothelial cell dysfunction. By the classic definition (reduced NO production), it isn't clear whether one of the fibronectin-binding integrins reduces NO production directly. Rather, the collagen binding integrins appear to promote NO production by shear stress when cells are on basement membrane proteins (Yurdagul et al., 2013). If you are referring to the rather loose definition of endothelial dysfunction to mean enhanced proinflammatory responses and permeability (better termed endothelial activation), then the integrin mediating shear stress-induced proinflammatory responses on fibronectin hasn't been published yet (but should be soon). However, a paper should come out in the next week or so (in ATVB) showing that alpha5beta1 mediates endothelial activation by oxidized LDL. As for the last part of the question (and can be induced by shear stress), endothelial cells only express beta1, beta3, and beta5. Activation of a2b1, a5b1, and avb3 by shear was published in MBoC in 2006. Activation of a6b1 (suggested by its ability to recruit Shc) was published in PNAS in 2001 (Jalali et al). Activation of avb5 has never been shown directly due to limitations in the reagents. I hope that helps, and if you have any more questions feel free to contact me.