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. Author manuscript; available in PMC: 2020 May 1.
Published in final edited form as: Matrix Biol. 2018 May 21;78-79:201–218. doi: 10.1016/j.matbio.2018.05.007

Figure 1. The CD44 / HA axis in the initiation of atherosclerosis.

Figure 1.

1A: During homeostasis, an intact, HMW HA-rich EC glycocalyx prevents adhesion of circulating leukocytes (monocytes and T cells). CD44 is inducible, but inactive. VSMCs are quiescent and contractile. 1B: Under pro-atherogenic conditions, high circulating levels of oxLDL promote EC activation and increased endothelial permeability by degrading the protective glycocalyx. EC adhesion molecule expression, including CD44, is increased, supporting adhesion of blood-borne leukocytes. Incoming active leukocyte CD44 bridges with its ligand HA on EC CD44 to facilitate leukocyte adhesion. The release of pro-inflammatory cytokines and chemokines (TNFα and IL-1β) also promote monocyte and T cell CD44 expression, as well as cell adhesion and extravasation into the sub-endothelium. VSMCs adopt a synthetic phenotype characterized by production of pro-inflammatory stimuli and increased ECM production.