Figure 4 Podocyte–endothelial cross talk and activation of heparanase

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Figure 4 Podocyte–endothelial cross talk and activation of heparanase Figure 4 | Podocyte–endothelial cross talk and activation of heparanase. a | The interactions between the endothelium and podocytes under physiological circumstances involve modification of the fenestrated endothelial glycocalyx-bearing phenotype in response to growth factor signalling from podocytes. The podocyte is anchored to the glomerular basement membrane (GBM) by binding to laminin 11, the proteoglycan agrin and α-actinin-4 (Ref. 136). b | Endothelial cell activation, such as occurs in the presence of cardiovascular risk factors and uraemic conditions, leads to oxidative stress137 and the production and secretion of factors such as endothelin 1 (ET1). In the podocyte, activation of the ETa receptor (ETaR) induces a feed-forward loop with stimulation of ET1 secretion and enhanced podocyte motility through activation of β-arrestin (not shown) and actin cytoskeletal rearrangements138. Simultaneously, ETaR signalling induces the formation of heparanase (HPSE), which in the presence of cathepsin L might further promote podocyte mobility and foot process effacement by degrading heparan sulfate chains, such as those attached to agrin, in the GBM, as well as induce loss of endothelial glycocalyx barrier function and facilitate the development of albuminuria33. Cathepsin L is a lysosomal cysteine protease that degrades numerous proteins, including components of the glomerular filtration barrier, such as CD2-associated protein, synaptopodin and dynamin, and can be secreted by activated podocytes139. Pro-HPSE, proheparanase. Rabelink, T. J. et al. (2017) Heparanase: roles in cell survival, extracellular matrix remodelling and the development of kidney disease Nat. Rev. Nephrol. doi:10.1038/nrneph.2017.6