On February 15th, at 11 am (BRT)
Speaker: Jacob van den Born, associate professor at State University of Groningen, University Medical Center Groningen, The Netherlands
Moderator: Mirian Hayashi, associate professor of Pharmacology at Unifesp, head of the Molecular Pharmacology Lab
Irrespective of the underlying disease, both acute and chronic kidney injury are associated by various tissue remodeling programs, such as inflammation, fibrosis, repair responses and (lymph-)angiogenesis aiming at renal recovery, however which upon chronicity lead to loss of renal function. Such tissue damage pathways are driven by a plethora of mediators produced mainly by activated endothelial and epithelial cells, and recruited inflammatory cells. The biological activity of many of these mediators, including growth factors, chemokines, complement factors and adhesion molecules is dependent on the binding with heparan sulfate proteoglycans (HSPGs). Upon injury, the kidney not only induces a number of mediators, but also starts up the HSPG turbo to accelerate tissue responses. In this Seminar I will highlight this paradigm by illustrating the amplifying role of renal HSPGs, especially tubular syndecan-1 in tubular regeneration and inflammation upon various forms of renal injury. Besides, we obtained ample evidence that tubular syndecan-1 can be exploited as receptive structure for cell penetrating peptides such as crotamine which enables specific targeting of renal proximal tubular epithelial cells. This approach allowed us to down-regulate complement activation on tubular epithelial cells, which might be of clinical importance.