“…Specifically, the glycocalyx has been shown to play a role in mechanosensing of smooth muscle cells and fibroblasts of the vascular system (Ainslie, Garanich et al 2005, Tarbell and Pahakis 2006, Shi and Tarbell 2011), and may be a relevant mechanism in the synovium during OA as changes occur to the interstitial matrix. Other work investigating the mechanisms addressed in this study already provide examples of potential strategies for controlling mechanosensitivity, such as manipulation of primary cilia length (Ou, Ruan et al 2009, Besschetnova, Kolpakova-Hart et al 2010) and gap junctional communication (Alves, Nihei et al 2000, Kurtenbach and Zoidl 2014). As such, we anticipate that a better understanding of these mechanisms will not only shed light on how the pathological sensitization of FLS to shear stress observed here contributes to the pathophysiology of OA, but point to therapeutic interventions that restore normal mechanosensitivity and hinder progression of the disease.…”